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Food and Nutrition Sciences, 2012, 3, 1100-1117
doi:10.4236/fns.2012.38146 Published Online August 2012 (http://www.SciRP.org/journal/fns)
Jamun (Syzygium cumini (L.)): A Review of Its Food and
Medicinal Uses
Shrikant Baslingappa Swami1*, Nayan Singh J. Thakor2, Meghatai M. Patil3, Parag M. Haldankar4
1Department of Agricultural Process Engineering, College of Agricultural Engineering and Technology, Dr. Balasaheb Sawant Kon-
kan Krishi Vidyapeeth, Dapoli, Ratnagiri, India; 2Department of Agricultural Process Engineering, College of Agricultural Engi-
neering and Technology, Dr. Balasaheb Sawant Konkan Krishi Vidyapeeth, Dapoli, Ratnagiri, India; 3NAIP-Kokum, Karonda,
Jamun and Jackfruit, Department of Agricultural Process Engineering, College of Agricultural Engineering and Technology, Dr.
Balasaheb Sawant Konkan Krishi Vidyapeeth, Dapoli, Ratnagiri, India; 4Department of Horticulture, College of Agriculture, Dr.
Balasaheb Sawant Konkan Krishi Vidyapeeth, Dapoli, Ratnagiri, India.
Email: *swami_shrikant1975@yahoo.co.in, nayan07@gmail.com, patil.megha2@gmail.com, parag5663@rediffmail.com
Received April 23rd, 2012; revised July 3rd, 2012; accepted July 10th, 2012
ABSTRACT
Eugenia jambolana Lam., commonly known as black plum or “jamun” is an important medicinal plant in various tradi-
tional systems of medicine. It is effective in the treatment of diabetes mellitus, inflammation, ulcers and diarrhea and
preclinical studies have also shown it to possess chemopreventive, radioprotective and antineoplastic properties. The
plant is rich in compounds containing anthocyanins, glucoside, ellagic acid, isoquercetin, kaemferol and myrecetin. The
seeds are claimed to contain alkaloid, jambosine, and glycoside jambolin or antimellin, which halts the diastatic conver-
sion of starch into sugar. The present review has been primed to describe the existing data on the information on tradi-
tional and medicinal use.
Keywords: Jamun-Syzygium cumini; Chemopreventive; Radioprotective; Antineoplastic Activities
1. Introduction
Syzygium cumini (Family Myrtaceae) is also known as
Syzygium jambolanum and Eugenia cumini. Other com-
mon names are Jambul, Black Plum, Java Plum, Indian
Blackberry, Jamblang, Jamun etc. Today these trees are
found growing throughout the Asian subcontinent, East-
ern Africa, South America, Madagascar and have also
naturalized to Florida and Hawaii in the United States of
America [1]. The tree fruits once in a year and the berries
are sweetish sour to taste. The ripe fruits are used for
health drinks, making preserves, squashes, jellies and
wine [1]. In association to its dietary use, all parts of the
tree and, importantly the seeds are used to treat a range
of ailments, the most important being diabetes mellitus
[2]. Different parts of the jambolan were also reported for
its antioxidant, anti-inflammatory, neuropsycho-phar-
macological, anti-microbial, anti-bacterial, anti-HIV, an-
tileishmanial and antifugal, nitric oxide scavenging, free
radical scavenging, anti-diarrheal, antifertility, anorexi-
genic, gastroprotective and anti-ulcerogenic and redio-
protective activities [2]. (Figure 1) shows the Jamun
fruit.
2. Composition of Fruit
Analyses of the fruit in the Philippines were reported in
1924 as follows: Waste, 25%; edible portion: water,
80.80%; ash, 0.70; protein, 0.81; sugar, 12.70 (fructose
and glucose; no sucrose); acidity (as sulphuric), 0.63%;
(as malic) 0.88% [3]. The following composition per 100
grams of edible portion was reported for fruits freshly
picked at the Lancetilla Experimental Garden, Honduras,
in 1948: Moisture, 85.8 gm; ether extract, 0.15 gm; crude
fiber, 0.3 gm; nitrogen, 0.129 gm; ash, 0.32 gm; calcium,
8.3 mg; phosphorus, 16.2 mg; iron, 1.62 mg; carotene,
0.004 mg; thiamine, 0.008 mg; riboflavin, 0.009 mg;
niacin, 0.290 mg; total ascorbic acid, 5.7 mg [4]. Virmani
gives the following analysis: specific gravity, 1.0184;
total acidity (as acetic acid), 5.33 per 100 cc; volatile
acidity (as acetic acid), 5.072 per 100 cc; fixed acidity,
0.275% as citric; total solids, 4.12 per 100 cc; ash, 0.42;
alkalinity of ash, 32.5 (N/10 alkali); nitrogen, 0.66131;
total sugars, 0.995; reducing sugars, 0.995; non-volatile
reducing sugars, 0.995; alcohol, 0.159% by weight; oxi-
dation value (KMnO4, 186.4); iodine value, 183.7; ester
value, 40.42. Other reported constituents of the seeds are:
protein (6.3 to 8.5%), fat (1.18%), crude fiber (16.9%),
*Corresponding author.
Copyright © 2012 SciRes. FNS
Jamun (Syzygium cumini (L.)): A Review of Its Food and Medicinal Uses 1101
Figure 1. Jamun fruit in a bunch.
ash (21.72%), calcium (0.41%), phosphorus (0.17%),
fatty acids (palmitic, stearic, oleic and linoleic), starch
(41%), dextrin (6.1%), a trace of phytosterol, and 6 to
19% tannin. [5] The fruits are avidly eaten by birds and
four footed animals (jackals and civets in India). In Aus-
tralia, they are a favorite food of the large bat called
“flying fox”. Analyses of the leaves show: crude protein
(9.1%), fat (4.3%), crude fiber (17.0%), ash (6.0%), cal-
cium (1.3%), phosphorus (0.19%) [6]. It consists mainly
of mono- or sesqui-terpene hydrocarbons which are
“very common in essential oils.” Constituents of Syzgium
cumini seeds are fatty oils (30 g/kg), including lauric
(2.8%), myristic (31.7%), palmitic (4.7%), stearic (6.5%),
oleic (32.2%), linoleic (16.1%), malvalic (1.2%), stercu-
lic (1.8%) and vernolic acid (3%) and phytosterols such
as β-sitosterol. Further constituents are tannins (6%),
predominantly corilagin, ellagitannins, ellagic acid, gal-
loyl-galactoside and gallic acid [7]. The leaf oil consists
of 16.91% octadecane, 9.98% nonacosane, 9.38% triac-
ontane, 7.38% octacosane, 4.86% Heptacosane, 4.25%
hexadecanoic acid and 4.02% eicosane. The seed oil
consists of 33.2% 1-chlorooctadecane, 9.24% tetratet-
racontane, 8.02% decahydro-8a-ethyl-1,1, 4a,6-tetrame-
thylnapahthalene, 5.29% 4-(2-2-dimethyl-6-6-methylene-
cyclohexyl) butanol, 5.15% Octadecane, 3.97% octaco-
sane, 1.72% heptacosane and 1.71% eicosane. [8]. Java
Plum consist of Energy 251 kJ (60 kcal), Carbohydrates
15.56 g, fat 0.23 g, Protein 0.72 g, water 83.13 g, Vita-
min A 3IU, Thiamine (vit B1) 0.006 mg (1%), Ribofla-
vin (vit. B2) 0.012 mg (1%), 0.260 mg (2%) Niacin (vit.
B3), 0.160 mg (3%) Pantothenic acid (B5), 0.038 mg (3%)
Vitamin B60.038 mg (3%), 14.3 mg (17%) Vitamin C, 19
mg (2%) Calcium, 0.19 mg (1%) Iron, 15 mg (4%)
Magnesium, 17 mg (2%) Phosphorus, 79 mg (2%) Potas-
sium, 14 mg (1%) Sodium [9]. The Fruit Contain 83.70 -
85.80 g moisture, 0.70 - 0.13 g protein, 0.15 - 0.30 g fat,
0.30 - 0.90 g crude fibre, 14.00 g carbohydrate, 0.32 -
0.40 h ash, 8.30 - 15.00 mg calcium, 35.00 mg magne-
sium, 15.00 - 16.20 mg phosphorus, 1.20 - 1.62 mg iron,
26.20 mg sodium, 55.00 mg potassium, 0.23 mg copper,
13.00 mg sulfur, 8.00 mh chlorine, 8. I.U vitamin A, 0.01 -
0.03 mg thiamine, 0.009 - 0.01 mg riboflavin, 0.20 - 0.29
mg niacin, 5.70 - 18.00 mg ascorbic acid, 7.00 mg chlo-
rine and 3.00 mcg folic acid per 100 g of edible portion
[10].
3. Food Uses
Good quality jambolan juice is excellent for sherbet [11,
12], syrup and “squash”. In India the latter is a bottled
drink prepared by cooking the crushed fruits for 5 to 10
minutes at 140˚F, pressing out the juice, combining it
with sugar and water and adding citric acid and sodium
benzoate as a preservative [13]. Jambolans of good size
and quality, having a sweet or sub acid flavor and a
minimum of astringency, are enjoyable raw and may be
made into tarts [14], sauces and jam. Astringent fruits are
improved in palatability by soaking them in salt water
[14] or pricking them, rubbing them with a little salt, and
letting them stand for an hour [15]. All but decidedly in
ferior fruits can be utilized for juice which is often com-
parable to grape juice [16]. When extracting juice from
cooked jambolans, it is recommended that it be allowed
to drain out without squeezing the fruit and it will thus be
less as tringent. The white-fleshed jambolan has adequate
pectin and makes a very stiff jelly unless cooking is brief
[17]. The more common purplefleshed yields richly col-
ored jelly [18] but is deficient in pectin and requires the
addition of a commercial jelling agent or must be com-
bined with pectin-rich fruits such as unripe or sour gua-
vas, or ketembillas [18]. In Goa and the Philippines [19],
jambolans are an important source of wine, resembling
Port [20]. Brandy and a distilled liquor called “jambava”
have also been made from the fermented fruit. Jambolan
vinegar, extensively made throughout India, is an attrac-
tive, clear purple, with a pleasant aroma and mild flavor.
4. Uses in Traditional Medicine
Traditionally the jambul fruits, leaves, seeds, and bark
are all used in ayurvedic medicine. The bark contains
tannins and carbohydrates, accounting for its long-term
use as an astringent to combat ailments like dysentery
[21]. A glycoside in the seed, jamboline, is considered to
have antidiabetic properties [22]. Older French research
shows that the seeds have a significant hypoglycemic
effect in diabetic rabbits [23]. The seeds have also shown
anti-inflammatory effects in rats and antioxidant proper-
Copyright © 2012 SciRes. FNS
Jamun (Syzygium cumini (L.)): A Review of Its Food and Medicinal Uses
1102
ties in diabetic rat [24]. Older reports from Indian medi-
cal journals suggest jambul seed and bark can be benefi-
cial in humans with diabetes. [25] Jamun fruit seeds and
pulp have been reported to serve various purposes in
diabetic patients, such as lowering blood glucose levels
and delaying diabetic complications including neuropa-
thy and cataracts [2,26]. Jamun is most often recognized
as an adjuvant therapy in type-2 diabetes. This has been
traced not only to its anthocyanin-rich, dark-purple fle-
shy pulp, but also to its seeds, which have been most
studied for their antidiabetic principles. Jamun seeds are
reported to be a rich source of ellagitannins (ETs), in-
cluding corilagin, 3,6-hexa hydroxyl diphenoyl glucose
and its isomer 4,6-hexahydroxy diphenoyl glucose, 1-
galloylglucose, 3-galloylglucose, gallic acid, and ellagic
acid (EA) [26]. This marker compound has anti-diabetic
activity. When alloxan induced diabetic rats were fed
with Jamun seed extract, the blood glucose, blood urea,
serum cholesterol and serum triglyceride levels were
found to decrease significantly [27]. Jamun fruit reduces
the sugar in the blood and is very good in the control of
diabetes. Its seeds contain Glucoside, Jamboline and El-
lagic acid, which are reported to have the ability to check
the conversion of starch into sugar in case of excess pro-
duction of glucose [27]. All parts of the jambolan can be
used medicinally and it has a long tradition in alternative
medicine. The plant has been viewed as an antidiabetic
plant since it became commercially available several
decades ago.
From all over the word, the fruits have been used for a
wide variety of ailments, including cough, diabetes, dys-
entery, inflammation and ringworm [28]. It is also an
ancient medicinal plant with an illustrious medical his-
tory and has been the subject of classical reviews for
over 100 years. It is widely distributed throughout India
and Ayurvedic medicine (Indian folk medicine) mentions
its use for the treatment of diabetic mellitus. Various
traditional practitioners in India use the different parts of
the plant in the treatment of diabetes, blisters in mouth,
cancer, colic, and diarrhea, digestive complaints, dysen-
tery, piles, pimples and stomachache [29]. During last
four decades, numerous folk medicinal reports on the
antidiabetic effects of this plant have been cited in the
literature. In Union medicine various parts of Jambolan
acts as liver tonic, enrich blood, strengthen teeth and
gums and form Good lotion for removing ringworm in-
fection of the head [30].
E. jambolana leaf extract showed hypoglycemic action
in diabetic rats [30]. The seed powder of E. jambolana is
reported to have hypoglycemic action in streptozotocin-
diabetic rats [31,32]. Its effect may be persistent, as in
one study, homeostasis was maintained in the rats for
two weeks after the cessation of treatment [32]. In al-
loxan-diabetic rabbits the water extract of E. jambolana
fruit pulp was more effective than the ethanol extract at
reducing fasting blood glucose and improving blood
glucose levels in the glucose tolerance test. E. jambolana
also increased blood insulin levels in both diabetic and
severely diabetic rabbits [33,34]. The inhibition of insu-
linase activity from liver and kidney by extract of
Eugenia jambolana also has been reported, which points
out to its extra-pancreatic mechanism [34].Another study
also found that E. jambolana seed extract reduced blood
glucose, glycosylated hemoglobin, and increased plasma
insulin [35]. E. jambolana fruit combined with bitter
melon decreased insulin levels that were raised in dia-
betic rats fed a fructose diet [36].
Jamun is most often recognized as an adjuvant therapy
in type-2 diabetes. This has been traced not only to its
anthocyanin-rich, dark-purple fleshy pulp, but also to its
seeds, which have been most studied for their antidia-
betic principles. Other reports from Indian medical jour-
nals suggest jambul seed and bark can be beneficial in
humans with diabetes [37]. When alloxan induced dia-
betic rats were fed with Jamun seed extract, the blood
glucose, blood urea, serum cholesterol and serum triglyc-
eride levels were found to decrease significantly [27].
Jamun fruit reduces the sugar in the blood and is very
good in the control of diabetes.
Ayurvedic texts suggest that 1 - 3 g of seed powder per
day is an average dose 44 additionally, Juice of ripe fruits
in the amount of 0.5 - 2 tsp (2.5 - 10 ml) at least three
times daily have been recommended for the treatment of
diabetes. Administration of 100 and 200 mg/kg body
weight of aqueous extract of Syzygium cumini pulp sig-
nificantly decreased the blood glucose level in the ex-
perimental rats suggesting that it has hypoglycemic prop-
erties. The decreased body weight in diabetic rats is due
to excessive breakdown of tissue proteins. Treatment
with Syzygium cumini improved body weight signifi-
cantly in a dose dependent manner, indicating prevention
of muscle wasting due to hyperglycemic condition.
5. Medicinal Properties
The jambolan has received far more recognition in folk
medicine and in the pharmaceutical trade than in any
other field. Medicinally, the fruit is stated to be astringent,
stomachic, carminative, antiscorbutic and diuretic [37].
Additionally, a fruit extract showed antimicrobial and
cytotoxic activities and may potentially be used on topi-
cal antimicrobial products. In comparison to other non-
traditional fruits jambolao showed considerable high
antioxidant activity, which can constituent such as an-
thocyanins, tannins and flavonols [38]. The anthocyanin
composition was characterised by the presence of 3,5-
diglucosides of five out of six aglycones commonly found
in foods [39]. Fruits contain many different kinds of
Copyright © 2012 SciRes. FNS
Jamun (Syzygium cumini (L.)): A Review of Its Food and Medicinal Uses
Copyright © 2012 SciRes. FNS
1103
anti-oxidant compounds, including flavonoids, phenolics,
carotenoids and vitamins, which are all considered bene-
ficial to human health, for decreasing the risk of degen-
erative diseases by reduction of oxidative stress, and for
the inhibition of macromolecular oxidation [40]. There is
a very high anthocyanin content in S. cumini fruits which
attributes to its antioxidant and free radical scavenging
activity. These pigments can be a good source of natural
food colourants for the food processing industries [41].
Fruit bark decoction for antiplasmodial activity was
performed, leading to the isolation of three known ellagic
acid derivatives (ellagic acid, ellagic acid 4-O-alpha-L-
2"-acetylrhamnopyranoside, 3-O-methylellagic acid 3'-O-
alpha-L-rhamnopyranoside), as well as the new deriva-
tive 3-O-methylellagic acid 3'-O-beta-D-glucopyranoside
[42]. 3-hydroxy androstane [16,17-C] (6'methyl, 2'-1-
hydroxyl-isopropene-1-yl) 4,5,6 H pyran present in Syzy-
gium cumini seed is one of the important marker com-
pound [43]. Phytochemical investigation of the stem bark
of Syzygium cumini (L.) Skeels (Myrtaceae) yielded four
new lignan derivatives characterised as (7α,8α,2'α)-3,4,
5-trimethoxy-7,3',1',9'-diepoxylignan (cuminiresinol), (7α,
7'α,8α,8'α)-3,4-dioxymethylene-3',4'-dimethoxy-7,9',7',9-
diepoxylignan-5'-ol (5'-hydroxy-methyl-piperitol), (7α,
7'α,8α,8'α)-3'-methoxy-9-oxo-7,9',7',9-diepoxylignan-3,4,
4'-triol or 3-demethyl-9-oxo-pinoresinol (syzygiresinol
A), (7α,7'α,8α,8'α)-9-oxo-7,9',7',9-diepoxylignan-3,4,3',4',
5'-pentaol or 3,3'-didemethyl-9-oxo-pinoresinol along
with the known lignans di-demethyl-5-hydroxypinores-
inol, dimethylpinoresinol, didemethoxypinoresinol, pi-
noresinol and 4'-methyl-5'-hydroxypinoresinol [44]. The
anthocyanins occur as 3,5-, but not 3-diglucosides, of
delphinidin, cyanidin, petunidin, peonidin, and malvidin.
This is the report to use a combination of spectrometric
and spectroscopic methods to identify unequivocally the
structures of E. jambolana fruit anthocyanins [45]. For
instance, flavonoids have been referred to as nature’s
biological response modifiers, because of their inherent
ability to modify the body’s reaction to allergies and vi-
rus and they showed their anti-allergic, anti-inflamma-
tory, anti-microbial and anti-cancer activities. Plant ster-
oids are known to be important for their cardiotonic ac-
tivities and also possess insecticidal and antimicrobial
properties. They are also used in nutrition, herbal medi-
cine and cosmetics [46]. Seed extracts of S. cumini, the
part most often used in Ayurvedic medicine, were previ-
ously shown to have high levels of total phenolics and
good activity in the trolox equivalent antioxidant capac-
ity (TEAC) and ferric reducing antioxidant power (FRAP)
antioxidant assays [47].
The juice of the ripe fruit, or a decoction of the fruit,
or jambolan vinegar, may be administered in India in
cases of enlargement of the spleen, chronic diarrhea and
urine retention [16,38]. Water-diluted juice is used as a
gargle for sore throat and as a lotion for ringworm of the
scalp [16,38]. Jambolan juice and mango juice, half and
half, quench thirst in diabetics [38]. The seeds (marketed
in-inch lengths) and the bark are official in the Dutch
[16]. They are much used in tropical medicine and are
shipped from India, Malaya and Polynesia, and to a small
extent from the West Indies [48], to pharmaceutical sup-
ply houses in Europe and England [49].
Studies in the past one decade have also shown that
Jamun possess antineoplastic [50]. Radioprotective [51-
54] and chemopreventive effects [55] all of which are
useful in the prevention and treatment of cancer. The
reasons for the myriad pharmacological effects are due to
the presence of diverse phytochemicals like flavonoids,
anthocyanins, terpenes [2] and are enlisted in Table 1.
Extracts of both, but especially the seeds, in liquid or
powdered form [61], are freely given orally, two or three
times a day to patients with diabetes mellitus or glyco-
suria [38]. In many cases, the blood sugar level report-
edly is quickly reduced and there are no ill effects [38].
Fresh seeds are considered superior to dried seeds [62].
Reduction of blood sugar was obtained in alloxan diabe-
tes in rabbits [62]. In experiments at the Central Drug
Research Institute, Lucknow, the dried alcoholic extract
Table 1. Phytochemicals present in the jamun plant.
Sr. No Plant part Chemicals present
1 Seeds
Jambosine, gallic acid, ellagic acid, corilagin, 3,6-hexahydroxy diphenoylglucose, 1-galloylglucose, 3-galloylglucose,
quercetin, β-sitoterol, 4,6 hexahydroxydiphenoylglucose, [2,56].
2 Stem bark
Friedelin, friedelan-3-α-ol, betulinic acid, β-sitosterol, kaempferol, β-sitosterol-Dglucoside, gallic acid, ellagic acid,
gallotannin and ellagitannin and myricetine [2,56].
3 Flowers Oleanolic acid, ellagic acids, isoquercetin, quercetin, kampferol and myricetin [2].
4 Fruit pulp Anthocyanins, delphinidin, petunidin, malvidin-diglucosides [2,57,58].
5 Leaves
β-sitosterol, betulinic acid, mycaminose, crategolic (maslinic) acid, n-hepatcosane, n-nonacosane, n-hentriacontane,
noctacosanol, n-triacontanol, n-dotricontanol, quercetin, myricetin, myricitrin and the flavonol glycosides myricetin
3-O-(4''-acetyl)-α Lrhamnopyranosides [2,59].
6 Essential oils α-terpeneol, myrtenol, eucarvone, muurolol, α-myrtenal, 1, 8-cineole, geranyl acetone, α-cadinol and pinocarvone [60].
Jamun (Syzygium cumini (L.)): A Review of Its Food and Medicinal Uses
1104
of jambolan seeds, given orally, reduced blood sugar and
glycosuria in patients [62]. Dr. Mukerji, in 1961, called
the results promising, though the action of the seed ex-
tract is milder than that of the synthetic anti-diabetics. He
holds that the bark extract affects the glycogenolysis and
glycogen storage in animals [38]. On the other hand,
Bhatnagar and co-workers, while screening the jambolan
with 174 other popular Indian medicinal plants, found no
physiological activity in the bark, which they collected in
the month of September [63]. Other reported constituents
of the seeds are: tannin, [16] to 19%; gallic acid, 1% to
2%; chlorophyll [55]; fatty acids (palmitic, stearic, oleic,
and linoleic) [16]; starch, 41% [15], dextrin, 6.1%; pro-
tein, 6.3% [15]; and a trace of phytosterol [16].The seeds
are claimed by some to contain a glycoside, jambolin
[16,55] or antimellin [62], which halts the diastatic con-
version of starch in to sugar [16]; also a resin yielding
phenolic substances named jambidol [15,16] and ellagic
acid [55], and an alkaloid, jambosine [61]. The bark con-
tains 8% to 19% tannin [15,55], gallic acid, 1.67% [16],
resin [64], small amounts of ellagic acid and myricetin
[65]. A decoction of the bark is taken internally for dys-
pepsia, dysentery and diarrhea and also serves as an en-
ema [16]. The dried and powdered seeds and root-bark
are similarly employed [16]. Powdered bark mixed with
curds is given in menorrhagia. Powdered jambolan and
mango seeds, with curds, are used, like the fruit juice, in
treating enlarged spleen and retained urine [38]. In India,
the seed powder is administered as an antidote for
strychnine poisoning [15]. The leaf juice is effective in
the treatment of dysentery [16], either alone or in com-
bination with the juice of mango or emblic leaves [38].
The leaves, steeped in alcohol, are prescribed in diabetes
[55]. Jambolan leaves may be helpful as poultices for
skin diseases [15,16]. The leaves yield 12% to 13% tan-
nin (by dry weight) (IS), also an essential oil containing
limeonene and dipentene (20% to 30%), about 40% of
sesquiterpene (cadeninic type) and a little azulenic ses-
quiterpene [62]. Bark decoctions are taken for asthma
and bron chitis [5] and are gargled or used as mouth
wash for the astringent effect on mouth ulcerations,
spongy gums [16] and for stomatitis [38]. Ashes of the
bark, mixed with water, are spread over local inflama-
tions; or, blended with oil, applied to burns [38].
In the year 2008, 12.7 million new cancer cases and
7.6 million cancer deaths occurred [66]. More worryingly,
predictions are that by the year 2020, the global inci-
dence of the cancer will increase by threefold, with a
disproportionate rise in cases from the developing world
countries that have limited resources to tackle the prob-
lem [67]. The conventional treatment modalities used in
treating cancer, the surgery, radiotherapy, hormone ther-
apy and chemotherapy remain prohibitively expensive to
the large number of population in the developing coun-
tries. With an expected rise in cancer incidence, the mor-
tality and associated morbidity will be enormous due to
the compromised financial condition of the patients [66,
67]. Since the dawn of civilization, herbal drugs have
been used in the ancient civilizations and their use in the
treatment of cancer is on a rise especially in the develop-
ing and underdeveloped countries primarily due to its
easy affordability, non toxic nature, easy acceptability,
less toxic or no toxic effects and easy availability. Plants
have been the main ingredients of various medications of
the traditional Indian system of medicine, the Ayurveda
and one such plant of immense importance is Eugenia
jambolana Lam (Syn. Syzygium cumini Skeels or Syzy-
gium jambolana Dc or Eugenia cuminii Druce). (Figure
1), colloquially known as Java plum, Portuguese plum,
Malabar plum, black plum, Indian blackberry, jaman,
jambu, jambul and jambool [68].
5.1. Chemopreventive Effects
Chemoprevention, a science that has emerged during the
three last decade, presents an alternative approach to re-
ducing mortality from cancer. Chemopreventive inter-
ventions may be applied at any time during carcinogene-
sis, from the initial molecular defect through the accu-
mulated molecular, cellular and histopathologic aberra-
tions that characterize disease progression before an in-
vasive and potentially metastatic stage [69]. It aims at
blocking, reversing, or delaying carcinogenesis before
the development of invasive disease by targeting key
molecular derangements using pharmacological or nutri-
tional agents [69]. Very recently [70] have also observed
that administration of the jamun extract (25 mg/kg body
weight/day) was effective in preventing benzo-a-pyrene-
induced forestomach carcinogenesis. Recently, [71] have
reported that jamun possess cancer chemopreventive
properties in the DMBA-induced croton oil promoted
two stage skin carcinogenesis in Swiss albino mice.
Feeding of 125 mg/kg body weight/animal/day of the
extract either during the perinitiation (i.e. 7 days before
and 7 days after the application of DMBA) or post-ini-
tiation (i.e. from the day of start of croton oil treatment
and continued till the end of the experiment) phases re-
duced the cumulative numbers of papillomas, the tumor
incidence and increased the average latency period when
compared with the control group (carcinogen alone) [71].
Jamun reduced the tumor incidence, tumor burden and
cumulative number of gastric carcinomas. Reports also
suggest that gallic acid, ellagic acid, flavonoids and an-
thocyanins (Figure 2) present in Jamun are reported to
prevent experimental carcinogenesis in various organs
(Table 2) and may have contributed to the anti-carcino-
genesis. Additionally, recent observations also suggest
that ellagitannin, a constituent of Jamun and its colonic
Copyright © 2012 SciRes. FNS
Jamun (Syzygium cumini (L.)): A Review of Its Food and Medicinal Uses 1105
Table 2. Phytochemicals of Jamun with reported chemopreventive effects
Sr. No Agent Chemopreventive effects and the mechanisms operating
1 Oleanolic acid
1) Inhibits tumor promotion in mouse skin [72]; 2) Inhibits azoxymethane (AOM)-induced colonic aberrant crypt foci
and multi-crypt aberrant crypt/foci in a dose dependent manner [73]; 3) Suppress preneoplastic lesions induced by 1,
2-dimethylhydrazine in rat colon [74].
2 Ellagic acid
1) Inhibitor of benzo[a]pyrene-induced pulmonary adenoma and 7,12-dimethyl benz[a]anthracene-induced skin
tumorigenesis in Swiss mice [75]; 2) Topical application [76] as well as oral feeding of ellagic acid [76] rendered
protection against 3-methylcholanthrene-induced skin tumorigenesis in mice and decreased tumor incidence, number of
tumors, tumors per mouse and tumors per tumor bearing animal [76,77]; 3) Topical application of ellagic acid and oral
before a tumor-initiating by B[a]P 7,8-diol-9,10-epoxide-2 and promotion with 12-O-tetradecanoylphorbol-13-acetate
inhibited the number of skin tumors per mouse [78]; 4) Ellagic acid applied topically to female CF-1 mice 20 min before
each 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment inhibit the inductions of epidermal ornithine decarboxylase
activity, hydroperoxide production and DNA synthesis, and also inhibit the promotion of skin papillomas and
carcinomas in the two-step initiation-promotion protocol [79]; 5) Topical application of ellagic acid simultaneously
with phorbol-12-myristate-13-acetate (PMA) or mezerein resulted in significant protection against 7,
12-dimethyl-benz[a]anthracene-induced skin tumors in mice [80]; 6) The levels of aryl hydrocarbon hydroxylase
(AHH) activity in skin and liver and the extent of 3H-BP-binding to skin, liver and lung DNA were decreased [76];
7) Is a potent inhibitor of benzo[a]pyrene metabolism and its subsequent glucuronidation, sulfation and covalent
binding to DNA in cultured BALB/C mouse keratinocytes [81]; 8) Inhibited the epidermal microsomal aryl hydrocarbon
hydroxylase (AHH) activity and of benzo[a]pyrene (BP)-binding to both calf thymus DNA in vitro and to epidermal
DNA in vivo [82].
3 Gallic acid
1) Inhibits the TPA-induced inductions of epidermal ornithine decarboxylase activity, hydroperoxide production and
DNA synthesis, and also inhibit the promotion of skin papillomas and carcinomas in the two-step initiationpromotion
protocol [79]; 2) Administering (0.3% to 1%) for twenty consecutive weeks from four weeks of age to the male TRAMP
mice (a transgenic mice develops prostate tumor) caused a decrease tumors with decreasing the proliferative index with
a concomitant increase in the apoptotic cells which were due to decrease in the expression of Cdc2, Cdk2, Cdk4, Cdk6,
cyclin B1 and E [83].
4 Quercetin
1) Possesses chemopreventive effects against 4-nitroquinoline 1-oxide-induced and its administration during both
initiation and post-initiation phases caused a significant reduction in the frequency of tongue carcinoma in rats. It
reduced the polyamine levels and the proliferation [84]; 2) Prevents N-nitrosodiethylamineinduced lung tumorigenesis
in mice [85]; 3) Prevents 20-methyl cholanthrene-induced cervical neoplasia in virgin Swiss albino mice by increasing
the antioxidant enzymes, decreasing DNA damage and he lipid peroxidation [86,87]; 4) Decreases DMBA-induced
DNA damage [88]; 5) In a bioengineered human gingival epithelial tissue, quercetin was observed to inhibit BaP-DNA
binding, a precursor for mutagenesis and carcinogenesis [89]; 6) Quercetin supplementation prevents
benzo(a)pyrene-induced carcinogenesis by modulating the antioxidants and decreasing lipid peroxidation, aryl
hydrocarbon hydroxylase, gamma glutamyl transpeptidase, 5’-nucleotidase, lactate dehydrogenase and adenosine
deaminase [90].
5 Myricetin
1) Inhibits epidermal growth factor (EGF)-activated cell transformation of JB6 cells by modulating DNA binding and
transcriptional activity of STAT3 [91,92], and mitogen-activated protein kinase (MEK) [93] and inhibitor of of
neoplastic cell transformation and MEK1 [94]; 2) Prevents TPA-induced transformation, PKC activation, and c-jun
expression in mouse fibroblast cells [95]; 3) Suppresses UVB-induced skin cancer by targeting Fyn in JB6 cells [96].
Inhibits Akt survival signaling and induces Bad-mediated apoptosis in immortalized human keratinocytes (HaCaT cells)
[97]; 4) Inhibits matrix metalloproteinase 2 protein expression and enzyme activity in colorectal carcinoma cells [98]
and also down-regulates phorbol ester-induced cyclooxygenase-2 expression in mouse epidermal cells by blocking
activation of nuclear factor kappa B [94]; 5) Inhibits polycyclic aromatic hydrocarbon-DNA adduct formation in
epidermis and lungs of SENCAR mice [99].
6 Kaempferol 1) Possess inhibitory effects on phosphatidylinositol 3-kinase and inhibits the neoplastic transformation [100].
7 Betulinic acid
1) Topical application of betulinic acid inhibited the TPA-induced inflammation and decreased the levels of ornithine
decarboxylase [101]; 2) Markedly inhibited the 7, 12-dimethylbenz[a]anthracene and TPA promoted skin tumor
formation in mice [101].
8 β- sitosterol
1) Topical application of β-sitosterol inhibited the TPA-induced inflammation [101]; 2) Induces dose-dependent growth
inhibition, induces apoptosis, suppresses the expression of β-catenin and PCNA antigens in human colon cancer cells
(COLO 320 DM cells) [102]; 3) β-sitosterol supplementation reduced the number of aberrant crypt and crypt
multiplicity in DMH-initiated rats in a dose-dependent manner with no toxic effects [102].
9 Delphinidin
1) Suppresses 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced cell transformation and activator protein-1
transactivation in the JB6 cells by blocking the phosphorylation of protein kinases in the extracellular signalregulated
protein kinase (ERK) and the c-Jun N-terminal kinase (JNK) signaling pathways [103]; 2) Possess chemopreventive
effects against prostate carcinogenesis in both in vitro and vivo study models [104]; 3) Suppresses ultraviolet B-induced
cyclooxygenases-2 expression through inhibition of MAPKK4 and PI-3 kinase [105].
Copyright © 2012 SciRes. FNS
Jamun (Syzygium cumini (L.)): A Review of Its Food and Medicinal Uses
1106
OH
OH
OH
OH
OH
O
O
OH
OH
OH
OH
OH
O
O
(a) (b)
OH
OH
OH
OH
OH
O
O
H
3
C
HO
CH
3
COOH
CH
3
CH
3
H
3
C
(c) (d)
OH
OH
OH
OH
O
OH
OH
OH
OH
OH
O
OH
(e) (f)
OH
OH
CH3
CH3
OH
OH
O
O
O
OH
OH
OCH
3
OH
OH
OH
O
(g) (h)
Copyright © 2012 SciRes. FNS
Jamun (Syzygium cumini (L.)): A Review of Its Food and Medicinal Uses
Copyright © 2012 SciRes. FNS
1107
OH
OH
OH
OH
OH
O
O
O
OH
OH
O
OH OH
(i) (j)
Figure 2. Structures of Phytochemicals in Jamun Reported to be of Use in the treatment of Cancer. (a) Myricetin; (b) Kaem-
pherol; (c) Quercetin; (d) Betulinic; (e) Anthocyanin; (f) Delphinidin; (g) Malvidian; (h) Petunidin; (i) Ellagic Acid; (j) Gallic
Acid.
metabolite, urolithin A inhibit want signaling crucial in
the process of colon carcinogenesis [106].
5.2. Radioprotective Effects
The affect felt by the normal cells are irreparable damage,
leading to the untoward effects forcing the physicians to
discontinue or reduce the treatment dose. In such situa-
tions, an agent that can render a therapeutic differential
between the cancer and normal cell will be highly bene-
ficial. Studies have shown that the intraperitoneal ad-
ministration of the hydroalcoholic extract of the Jamun
seed and the dichloromethane extract of Jamun leaf pos-
sess radioprotective effects [107]. Therapeutic differen-
tial may be achieved with chemical compounds that may
selectively protect the normal cells from the deleterious
effects of radiation termed as radio protectors. Since the
observations of [108] that the natural amino acid cysteine
protected mice against radiation-induced sickness and
mortality, many compounds with varied pharmacological
properties have been synthesized and evaluated for their
radioprotective effects. Pretreatment with hydroalcoholic
extract of jamun seeds (5 to 160 mg/kg body weight) for
five consecutive days before exposure to supralethal dose
of radiation (10 Gy) protected mice against the radiation-
induced sickness and mortality. The best effect was ob-
served at 80 mg/kg but only when administered through
the intraperitoneal route as 50% of the animals survived
when compare to 22% in the oral route and none in the
radiation alone cohorts. The intraperitoneal administra-
tion of the organic extract (dichloromethane-methane) of
leaves (5, 10, 20, 30, 40, 50, 60 and 80 mg/kg b. wt.) for
five days before irradiation was also observed to be ef-
fective in preventing the radiation-induced sickness and
mortality in mice. Histopathological investigations showed
that Jamun leaf treatment before radiation elevated the
villus height, the number of crypts and reduced the gob-
let and dead cells when compared with the concurrent
irradiation control. The recovery and regeneration was
faster in Jamun pretreated animals than the irradiation
alone. Jamun extracts also provides protection to the
DNA against the radiation-induced DNA damage (ex-
plained later). The phytochemicals ellagic acid, gallic
acid, quercetin and oleanolic acid (Figure 2) present in
Jamun also possess radioprotective effects (addressed in
Table 3).
5.3. Antineoplastic Effects of Jamun
Chemotherapy has been an important modality in cancer
treatment for more than five decades and is an obligatory
treatment modality when metastasis has ensued. De-
pending on the clinical stage and the patient compliance,
chemotherapy is used either alone or in combination with
radiation and surgery [118]. Studies suggest that of all
the antineoplastic drugs being used nearly 47% of the
drugs are from natural sources [119]. With regard to
Jamun many compounds exert beneficial influence (Fig-
ure 2 and Table 4).
In vitro studies by [177] have shown that whole Jamun
extract possess cytotoxic effects on the cultured human
cervical cancer cells, the HeLa (HPV-18 positive) and
SiHa (HPV-16 positive). The extract caused a concentra-
tion dependent cell death with the effect being more
pronounced in the HeLa than SiHa cells [177]. Addition-
ally, both crude as well as the methanolic extracts of the
pulp caused a time dependent increase in apoptosis when
cultured with 80% concentration of the extracts. The
crude extract was observed to be better than the metha-
nolic extract in both the cell lines [177]. In a study that
has wide clinical implications, recent studies by [57]
have shown that the standardized Jamun fruit extract
possess antiproliferative and pro-apoptotic effects in the
estrogen dependent aromatase positive (MCF-7aro), and
estrogen independent (MDA-MB-231) breast cancer cells.
The extract was highly effective against MCF-7aro and
the IC50 was observed to be 27 μg/ml to that of 40
μg/ml in MDAMB-231. Most importantly, at equivalent
Jamun (Syzygium cumini (L.)): A Review of Its Food and Medicinal Uses
1108
Table 3. Phytochemicals of Jamun with reported radioprotective activities
Sr. No Agent Phytochemicals radioprotective effects and the mechanisms operating
1 Oleanolic acid 1) Inhibits the growth of ascitic tumors and enhances the recovery of hematopoietic system in irradiated mice [109].
2 Quercetin
1) Protected yeast cells from γ-radiation damage by reducing DNA damage [110]; 2) Effective inprotecting against
γ-radiation-induced DNA damage to the human peripheral blood lymphocytes in vitro [104, and plasmid DNA [111].
The protective mechanisms were mediated by the antioxidant and inhibition of lipid peroxides [111]; 3) Intraperitoneal
administration of quercetin 100 mg·kg/kg for 3 consecutive days before and/or after irradiation prevented radiation
induced DNA damage in WBC of mice. Pronounced effects were when querecetin was administered before radiation
[112,113]
3 Gallic acid 1) Inhibits radiation-induced damage to DNA and lipid peroxidation in both in vitro and in vivo conditions [114].
4 Ellagic acid
1) Protects yeast cells from γ-radiation-induced damage by reducing DNA damage [115]; 2) Inhibits γ-radiation induced
lipid peroxidation in a concentration-dependent manner in vitro [116]; 3) Enhances the cytotoxic effects of radiation in
neoplastic cells (Ehrlich ascites carcinoma and Hela) by inducing free radicals, reducing antioxidant enzymes and
altering the mitochondrial potential, but protects the normal cells (splenic lymphocytes) of tumor-bearing mice against
the radiation damage [117].
Table 4. Phytochemicals in Jamun with reported antineoplastic activities.
Sr. No Agent Antineoplastic activity and the mechanisms operating
1 Oleanolic acid
1) Causes a dose and a time dependent cell kill of the human colon carcinoma cell line HCT15. Inhibits proliferation and
arrested the cells in G0/G1 phase [120]; 2) Induces apoptosis in human leukemia cells HL60 through caspase activation
[121]; 3) Selectively inhibits growth of ras oncogene-transformed R6 cells [122]; 4) Induces apoptosis in human liver
cancer HepG2, Hep3B, Huh7 and HA22T cell lines [123]; 5) Inhibits growth of ascitic tumors in mice [108].
2 Quercetin
1) Causes dose-dependent cell kill, chromatin condensation in the colon cancer cells (Caco-2 and HT-29) [124]; 2)
Potentiates inhibitory effect of a non-toxic dose of cisplatin, inhibits lung colonization of B16-BL6 colonies and in a
dose-dependent manner [125]; 3) Inhibits the growth of the highly aggressive PC-3 prostate cancer cell line and the
moderately aggressive DU-145 prostate cancer cell line, but ineffective on the poorly aggressive LNCaP prostate cancer
cell line or the normal fibroblast cell line BG-9 [126]; 4) Inhibits expression of specific oncogenes and genes controlling
G1, S, G2 and M phases of the cell cycle. It also up-regulated the expression of several tumor suppressor genes [126];
5) Down regulates gelatinases A and B (matrixmetalloproteinases 2 and 9) in the human prostate cancer cells (PC-3) in
vitro [127].
3 Kaempferol
1) Inhibits proliferation and induces cell death in human glioma cells through caspase-dependent mechanisms involving
down-regulation of XIAP and surviving regulating by ERK and Akt [128]; 2) Mediates p53-dependent growth inhibition
and induces apoptosis in human HCT116 colon cancer cell line by affecting Bcl-2 family proteins, PUMA and inducing
ATM and H2AX phosphorylation [129]; 3) Induces apoptosis in various oral cancer cell lines (SCC-1483, SCC-25 and
SCC-QLL1) through the caspase-3-dependent pathway [130]; 4) Induces apoptosis via endoplasmic reticulum stress and
mitochondria dependent pathway in human osteosarcoma U-2 OS cells [131].
4 Myricetin
1) Induce apoptosis in HT-29 [132], Caco-2 cells [132], MCF7 (Rodgers and Grant, 1998), Jurkat T cells [133], OE33
[134] and HepG-2 [135]; 2) Inhibits proliferation, causes G2/M and S phase arrest and induces mitochondria-mediated
apoptosis by activation of caspase 3, 9 of HepG-2 [135]; 3) Possess cytotoxic effects against the OE33 (human oeso-
phageal adenocarcinoma cell line), causes G2/M cell cycle arrest by up-regulation of GADD45beta and 14-3-3sigma and
down-regulation of cyclin B1; and p53-independent mitochondrial-mediated apoptosis through up-regulation of PIG3
and cleavage of caspase-9 and 3 [134]; 4) Possess moderate proteasome inhibitory effects and induce apoptosis in the
human leukemia cells Jurkat T cells [135].
5 Gallic acid
1) Induces apoptosis in human prostate LNCaP cells [136]; 2) Induces cytotoxic effects on DU145 prostate cancer
cells, through generation of reactive oxygen species and mitochondria-mediated apoptosis [137]; 3) Blocks the growth
of DU145 cells at G2/M phases by activating Chk1 and Chk2 and inhibiting Cdc25C and Cdc2 activities [137]; 4)
Inactivates phosphorylation of cdc25A/cdc25Ccdc2 via ATM-Chk2 activation, leading to cell cycle arrest, and induces
apoptosis in human prostate carcinoma DU145 cells [138]; 5) Possess anti-proliferative, pro-apoptotic and
anti-tumorigenic effects against human prostate cells DU145 and 22Rv1 in vitro and in nude mice [139]; 6) Synergizes
with doxorubicin to suppress the growth of DU145 cells [136]; 7) Induces apoptosis through both caspase-dependent
and -independent pathways in the in A375.S2 human melanoma cells [140]; 8) Possesses in vitro anticancer effects
against the human prostate cancer cells [141]
6 Betulinic acid
1) Is effective against a variety of cancer types but relatively safe to the normal cells and tissue at equal concentrations
[141]; 2) Induces potent effect on growth inhibition, G2/M cell cycle arrest and triggers apoptosis in the human gastric
adenocarcinoma AGS cells in vitro, possibly by the down-regulation of Hiwi and its downstream target Cyclin B1
expression [142]; 3) Causes a dose dependent cytotoxic effect on the rhabdomyosarcoma cell line RMS by inducing
apoptosis through the intrinsic mitochondrial pathway. It also decreased GLI1, GLI2, PTCH1, and IGF2 expression as
well as hedgehog-response in vitro. It also caused retarded the growth of RMS-13 xenografts by causing apoptosis and
down-regulating GLI1 expression without affecting the microvascular density, cell proliferation, and myogenic
differentiation unaffected [143]; 4) Induces apoptosis through the mitochondrial pathway and inducing cytochrome c
Copyright © 2012 SciRes. FNS
Jamun (Syzygium cumini (L.)): A Review of Its Food and Medicinal Uses 1109
Continued
6 Betulinic acid
release directly via PT Pore. The process is momentarily inhibited by the anti-apoptotic members of the Bcl-2 family, and
is observed to be independent of Bax and Bak [144]; 5) Induces cancer cell death by apoptosis through the mitochondrial
pathway and also sensitizes the anticancer effects of 5-fluorouracil (SNU-C5/5FU-R), irinotecan (SNU-C5/IRT-R) and
oxaliplatin (SNU-C5/OXT-R) in chemoresistant colon cancer cell lines derived from the colon adenocarcinoma cell line
(SNU-C5/WT) (Jung et al., 2007); 6) Effective against the androgen-refractory human prostate carcinoma PC-3 cells and
this it achieves by inhibiting DNA binding, reduced nuclear levels of the NF-kappaB/p65, decreased IKK activity and
phosphorylation of IkappaBalpha at serine 32/36 followed by its degradation [145]; 7) Inhibits the proliferation of Jurkat
cells by regulating the cell cycle and arresting the cells at G0/G1 phase by down-regulating the expression of cyclin D3. It
also induces apoptosis through the Bcl-xl [145].
7 1,8-Cineole 1) Induces apoptosis in human leukemia Molt 4B and HL-60 cells, but not in human stomach cancer KATO III cells [146].
8 β-Sitosterol
1) Inhibits growth of HT-29 human colon cancer cells by activating the sphingomyelin cycle [147]; 2) Activates the
sphingomyelin cycle and induces apoptosis in LNCaP human prostate cancer cells; 3) Stimulates apoptosis in
MDA-MB-231 human breast cancer cells in vitro and inhibits growth and metastasis of MDA-MB-231 in SCID mice
[148-154]; 4) Inhibits growth and metastasis of human prostate cancer PC-3 cells, in vitro and in SCID mice [154]; 5)
Induces apoptosis by stimulating Bax and activation of caspases in the HT116 human colon cancer cells [155]; 6) Induces
apoptosis in MCA-102 murine fibrosarcoma cells by activation of ERK and the downregulation of Akt [156,157]; 7)
Inhibits cell growth and induces apoptosis in SGC-7901 human stomach cancer cells in vitro [158]; 8) Induces significant
dose-dependent growth inhibition, suppressed expression of beta-catenin and PCNA antigens in human colon cancer cells
COLO 320 cells in vitro. Feeding beta-sitosterol also caused a dose dependent reduction in the number of aberrant crypt
and crypt multiplicity in DMH-initiated rats with no toxic effects [102].
9 Delphinidin
1) Inhibits proliferation of human cancer cell lines MCF-7 (breast), SF-268 (central nervous system, CNS), HCT-116
(colon), and NCI-H460 (lung) [159]; 2) Induce cell cycle perturbations and apoptosis in human cell lines [160]; 3) Inhibits
the growth and induced apoptosis in HL60 cells (Katsube et al., 2003). Inhibited the growth of HCT116 cells [161]; 4)
Preferentially inhibited the growth of the human vulva carcinoma cell line A431 by affecting the epidermal growth-factor
receptor (EGFR), the tyrosine kinase activity and inhibited the activation of the GAL4-Elk-1 [162]; 5) Potent inducer of
intracellular hydrogen peroxide and causes apoptosis in a time- and dose-dependent manner. Stimulates JNK pathway
activation including JNK phosphorylation and c-jun gene expression, and activates caspase-3 and causes DNA
fragmentation in HL-60 cells [163]; 6) Reduces cell growth, is potent EGFR- or PDE-inhibitor and the CAMP hydrolysis
[164]; 7) Inhibits cell proliferation of human cancer cell lines, AGS (stomach), HCT-116 (colon), MCF-7 (breast), NCI
H460 (lung), and SF-268 [165]; 8) Possess strong growth inhibitory effects against human hepatoma HepG(2), but were
less effective against Hep3B, induced apoptotic cell death by up-regulation of Bax and down-regulation of Bcl-2 protein
(Yeh et al., 2005); 9) Induces apoptosis in HT-29 cells [166]; 10) Inhibits HGF-mediated membrane translocation of
PKCalpha, decreases phosphorylation of STAT3. Repress HGF-activated NFkB transcription, phosphorylation of
IKKalpha/beta and IkappaBalpha, and activation and nuclear translocation of NFkappaB/p65 [167]; 11) Suppress the
phosphorylation of the epidermal growth factor receptor (EGFR) in human colon carcinoma cell line (HT29), human
vulva carcinoma cell line A431 [168]; 12) Treatment to AU-565 cells, a EGFR in the positive breast cancer cells inhibited
the phosphorylation of EGFR, activation of PI3K, phosphorylation of AKT and MAPK, inhibited EGF-induced
autophosphorylation of EGFR, AKT and MAPK, activation of PI3K and cell invasion [169]; 13) Treatment of in human
colon cancer HCT116 cells with delphinidin decrease cell viability; induces apoptosis; cleaves PARP; activates caspases-3,
-8, and -9; increase Bax with a concomitant decrease in Bcl-2 protein; causes G2/M cell cycle arrest; inhibited IKKalpha,
phosphorylation and degradation of Ikappa Balpha, phosphorylation of NF-kappaB/p65 at Ser(536), nuclear translocation
of NF-kappaB/p65, NFkappaB/ p65 DNA binding activity, and transcriptional activation of NF-kappaB [170]; 14)
Treatment to human PCa LNCaP, C4-2, 22Rnu1, and PC3 cells resulted in a dose-dependent inhibition of cell growth
without having any substantial effect on normal human prostate epithelial cells. It caused a dose-dependent induction of
apoptosis and arrest of cells in G2-M phase, decrease in phosphorylation of IkappaB kinase gamma, phosphorylation of
nuclear factor-kappaB (NF-kappaB) inhibitory protein IkappaBalpha, phosphorylation of NF-kappaB/p65 at Ser(536) and
NF-kappaB/p50 at Ser(529), NF-kappaB/p65 nuclear translocation, and NF-kappaB DNA binding activity. It also inhibited
the tumor growth in athymic nude mice implanted with PC3 cells by causing decrease in the expression of
NF-kappaB/p65, Bcl2, Ki67, and PCNA [171]; 15) Attenuates neoplastic transformation in JB6 Cl41 mouse epidermal
cells by blocking Raf/mitogen-activated protein kinase kinase/ extracellular signal-regulated kinase signaling [172]; 16)
Possess antiproliferative, anti-invasive and apoptotic effects in human hepatoma Hep3B cells. It also caused concentration
dependent increase in the sub-G1 fraction, mitochondrial dysfunction and reduction in antiapoptotic proteins (Bcl-2, xIAP,
cIAP-1, and cIAP-2) [173]; 17) Selectively causes cytotoxic effects on the LoVo and LoVo/ADR, human colorectal cancer
cell lines; while the non cancerous cells Caco-2 were unaffected [174]; 18) Inhibits receptor tyrosine kinases of the ErbB
and VEGFR family [175].
10 Petunidin 1) Induces apoptosis in HT-29 cells [166]; 2) Inhibits the human breast cancer (MCF-7) cell growth [165].
11 Malvidin
1) Inhibits growth and induced apoptosis in HL60 cells [161]; 2) Induces cell cycle perturbations and apoptosis in human
cell lines [160]; 3) Reduces cell growth, is potent EGFR- or PDE-inhibitors and effectively inhibited the CAMP
hydrolysis [164]; 4) Malvidin inhibited AGS (stomach), HCT-116 (colon), MCF-7 (breast), NCI and H460 (lung) [165];
5) Exhibits strong growth inhibitory effects against human hepatoma HepG(2), but were less effective against Hep3B
[176]; 6) Induces apoptosis in HT-29 cells [166]; 7) Effective on metastatic colorectal cancer cell lines LoVo and
LoVo/ADR [174]; 8) Possess antiproliferative, anti-invasive and apoptotic effects in human hepatoma Hep3B cells. It also
caused concentration dependent increase in the sub-G1 fraction, mitochondrial dysfunction and reduction in antiapoptotic
proteins (Bcl-2, xIAP, cIAP-1, and cIAP-2) [173]; 9) Possess good COX-1 and -2 inhibitory activities [159].
Copyright © 2012 SciRes. FNS
Jamun (Syzygium cumini (L.)): A Review of Its Food and Medicinal Uses
Copyright © 2012 SciRes. FNS
1110
concentrations the extract was relatively non toxic as it
did not induce cell death and apoptosis in the normal/
nontumorigenic (MCF-10A) breast cell line (IC50 > 100
μg/ml). Together these results clearly indicate that at
supra dietary levels the fruit pulp extract possesses selec-
tive antineoplastic effects against breast cancer [57].
6. Conclusion
Jambolan is traditionally used for the treatment of vari-
ous diseases especially diabetes and related complica-
tions. Most pharmacological works on diabetes were
carried out with seeds but the pharmacological potential
of the other parts of the plant is required to explore in
detail. With regard to the antineoplastic activities studies
suggest that Jamun is selective in its action in breast
cancer cells. The effect of Jamun and its phytochemicals
should also be investigated for its chemopreventive ef-
fects in other models of carcinogens, that includes
chemical, radiation and viral carcinogenesis models.
Mechanistic studies responsible for the chemopreventive
and radioprotective effects are also lacking and need to
be studied in detail. Based on these facts, this review
highlights the role of jambolan in various treatments and
recommend that further phytochemical and clinical re-
search should be done on this traditional medicinal plant
for the discovery of safer drugs. Studies should also be
on understanding which of the phytochemicals are re-
sponsible for the observed beneficially effects and if ef-
fective, their mechanism of action.
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