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Current Trends in Pharmacy and Pharmaceutical Chemistry 2022;4(4):158–164
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Review Article
Ethnopharmacological review of ginger for anticancer activity
Amit Gajanan Nerkar
1,2,3,*, Srushti Ghadge1
1Dept. of Pharmacy, CAYMET’s Siddhant College of Pharmacy, Sudumbare, Pune, Maharashtra, India
2Founder and Director, Ateos Foundation of Science Education and Research, Pune, Maharashtra, India
3Founder and Director, Carolene Therapeutics, Pvt. Ltd, Aurangabad, Maharashtra, India
ARTICLE INFO
Article history:
Received 24-10-2022
Accepted 16-11-2022
Available online 21-11-2022
Keywords:
Ginger
Ethnopharmacology
Anticancer activity
Pharmacognosy
Zingiber Officinale
ABSTRACT
Zingiber officinale is a plant found locally in India that has been widely used as a flavouring agent in
savoury dishes such as curries and sweets such as cakes and cookies, alcoholic beverages as well as in
alcoholic beverages. like in tea. Ginger is a well-known herb, commonly used in traditional medicine all
over the world. Ginger has been used for thousands of years to treat colds, nausea, arthritis, migraines, and
high blood pressure. The many pharmacological activities of ginger are antiemetic, antidiabetic, analgesic,
anti-inflammatory, anticancer, antioxidant, anticoagulant, antibacterial, anti-inflammatory, estrogenic and
cardiovascular activities. Chemical irritants and an unsaturated phenolic ketone liquid C17H24O3 are
responsible for the spicy taste of ginger. The main components of ginger are aromatic essential
oils, antioxidants and pungent resins. These aromatic or pungent compounds have been identified as
C6H5C(O)CH3, known as a chemical irritant, liquid unsaturated phenolic ketones C17H24O3 and
Vanillylacetone.
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1. Introduction
Ginger (Canton ginger) belongs to the family
Zingiberacea.1It is herbaceous perennial plant.2It is
commonly used as a spice and medicinal plant.2The part
of the plant used is the rhizome. The plant produces an
orchid-like flower with purple-flecked yellow-green petals.
Ginger (Zingiber officinale (L.) Roscoe) has been used as
a spice for over 2000 years.3Ginger contains up to 3% of
the essential oils responsible for the aroma of the spice.4
In India and countries with hot and humid climates, ginger
is consumed in large quantities and is good for digestive
problems.5Ginger belongs to the plant family that includes
cardamom and turmeric. Its spicy taste is mainly due to the
presence of ketones, especially ginger root, which seems
to be the main component of ginger studied in most of
* Corresponding author.
E-mail address:dragnerkar@gmail.com (A. G. Nerkar).
the health-related scientific studies.6The rhizome, which
is the horizontal stem from which the roots grow, is the
main part of the ginger that is consumed. Ginger’s current
name comes from the Middle English gingivere, but the
spice dates back more than 3,000 years to the Sanskrit word
srngaveram, meaning "horny root", based on its shape.7
In Greek it is called ziggiberis, and in Latin zinziberi.
Interestingly, ginger does not grow in the wild and its true
origin is uncertain. The Indians and Chinese are said to
have produced ginger as a root tonic for over 5000 years to
cure many ailments, and the herb is now grown throughout
the humid tropics. India is the largest ginger producer.
Ginger was used as a salting agent long before official
history was recorded. It was an extremely important trade
item and was exported from India to the Roman Empire
over 2000 years ago, where it was particularly prized for
its healing properties. Ginger continued to be a much
https://doi.org/10.18231/j.ctppc.2022.028
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Nerkar and Ghadge / Current Trends in Pharmacy and Pharmaceutical Chemistry 2022;4(4):158–164 159
sought-after commodity in Europe even after the fall of the
Roman Empire, with Arab traders controlling the trade in
ginger and other spices for centuries.8In the 13th and 14th
centuries, the value of a pound of ginger was equivalent to
the price of a sheep. Raw and preserved ginger was brought
to Europe in the Middle Ages, where it was included in
the official accumulations of various countries. During
the Middle Ages, it was imported in canned form for use
in sweets. Queen Elizabeth I of England is credited with
inventing the gingerbread man, which has become a popular
Christmas treat.9
1.1. Classification
Taxonomic Dry ginger
plant
Domain Eukaryota
Kingdom Plantae
Phylum Spermatophyta
Subphylum Angiosperms
Class Monocotyledon
Order Zingiberales
Family Zingiberacea
Genus Ginger
Species Zingiber
officinale
1.2. Active Constituents
At least 115 components of fresh and dried ginger varieties
have been identified through multiple analytical procedures.
Ginger has many active components, such as phenolics
and terpenoids.10 The phenolic compounds in ginger are
mainly ginger root,6-shogaol and paradols. In fresh ginger,
ginger root has the main polyphenols such as 6-gingerol,
8-gingerol and 10-gingerol. Ginger root is the major
constituent of fresh ginger and was found to be slightly
reduced in dried ginger, while concentrations of6-shogaol,
which is the main dehydration product of gingerol, were
more abundant11 in drier ginger than fresh ginger. At least
31 compounds related to gingerol have been identified from
crude methanolic extracts of fresh ginger rhizomes (Jiang,
Solyom et al. 2005). Ginger is rich in active ingredients,
such as phenolics and saponins. Ginger has been subdivided
into at least 14 bioactive compounds, including z4-
gingerol,6-gingerol,8-gingerol,10 -gingerol, 6-paradol, 12
-shogaol,6-shogaol, 1-dehydro-10 -gingerdione, 10 -
gingerdione, 3-heptanone, 5-hydroxy-1,7-bis (4-hydroxy-
3-methoxyphenyl), C21H24O6, linear log lheptanoids, 1,
7-bis- (4′hydroxyl-3′metoxyphenyl)-5-methoxyhepthan-
3-one and metoxy-10 –gingerol.13. The proportions of
each individual ingredient in a sample of ginger depend
on the country of origin, commercial processor and fresh,
dried or processed ginger.14 Among the pungent bioactive
components of Jamaican ginger, including,6-, 8-, and 10
roots and6-shogaol,6-gingerol appears to be the pungent
compound. has the most abundant biological activity in
most of the petroleum resins.12 Although phylogenetic
analysis revealed that all ginger samples from different
geographical origins were genetically indistinguishable,
metabolic profiling revealed quantitative differences. on
the content of6-,8– and10 - ginger root. 15 An evaluation
of the concentrations of6-,8-, and 10 root and 6-shogaol
in 10 different ginger root dietary supplements randomly
purchased from pharmacies. Various drug and grocery
stores, natural foods have given amazing results. Perhaps
unsurprisingly, the amounts of these active ingredients
vary widely, from none or very small amounts to several
milligrams per gram. In addition, the recommended dietary
intake ranges from about 250 mg to 4.8 g/day. The basis
for the wide dosage range is unclear. These studies show
that ginger contains many bioactive compounds and
standardization of the content is very lacking.16
2. Ethnopharmacological review of anticancer activity
Vallinoids in Ginger possess anticancer activities. Vallinoids
are certain pungent active constituents like6-gingerol
and6-paradol, and some other constituents like6-shogaol,
vanillylacetone etc. It was demonstrated that6-ginerol, 6
-shogaol and vanillyacetone possess anti-angiogenesis
dependent human diseases properties that helps to fight
the cancer. There has been substantial research on the
anticancer activities of active constituents of ginger and its
various components and were reviewed the properties of
giner and its chemoprophylaxis effects of numerous dietary
and medicinal plants. Studies were conducted on anticancer
activities of various parts and forms of ginger especially6-
gingerol;6-shogaol, especially6-shogaol; and zerumbone,
a sesquiglucoside compound derived from ginger and a
number of minor components and metabolites.17–21 The
effectiveness of ginger in preventing or suppressing cancer
growth has been examined in a variety of cancer types
such as lymphoma, hepatoma, colorectal cancer, breast
cancer, skin cancer, liver cancer, and bladder cancer. The
mechanisms showed the anticancer activities of ginger and
its components include antioxidant activity and induction
of apoptosis, decrease proliferation, cause cell-cycle arrest,
and suppress activator protein 1 (AP-1) and NF-κB/COX-2
indicating pathways.22
The antitumor activities of6-gingerol and zerumbone are
related to their antioxidant activities. Several components
of ginger were reported to have potent anticancer promoter
activity based on their ability to inhibit TPA-induced
Epstein-Barr virus early antigen (EBV-EA) in B
lymphocytes in humans.6,23 -Gingerol was reported to
block the potent invasive capacity of reactive oxygen
species of AH109A liver cancer cells ascites by reducing
peroxide levels.24 In normal mouse RL34 hepatic epithelial
160 Nerkar and Ghadge / Current Trends in Pharmacy and Pharmaceutical Chemistry 2022;4(4):158–164
Table 1: It shows anticancer activity of ginger with mechanism of action
Compound Name Cancer Mechanism Cell Lines/System
Ginger extract Liver cancer Reduced the elevated expression of TNF
–αand NF-kB and tumor growth
In-vitro
Ginger-whole
and6-gingerol
Non-small-cell lung cancer cells Release of cytochrome c In-vitro
β- Elemence Non-small-cell lung cancer cells Release of cyctocrome c In-vitro
6-gingerol Breast cancer Inhibites cell adhesion invasion motility In-vitro
Skin cancer Enhance apoptosis Mouse
Colon cancer Inhibition of leukotriene activity Mice
Lung and colon cancer Suppresses modulatorymechnism of
growth and induces apoptosis, Reduces
expression of NF-kB
Mouse
Zerumbone Colon cancer Activation of extraction signal-regulated
kinase 1
2p38 mitogen-activated protein
kinase
In-vitro
Osteoclastogenesis Blocks NF-kappa B expression. Mouse nonocyte
6-Shogaol Lungs cancer Inhibition of AKT In-vitro
6-Shogaol Breast cancer Anti-metastasis In-vitro
Enone-diary1
heptanoid,6-shogaol,10-
gingerol
Liver/against nine human tumor
cell (lines)
Inhibition of lipid peroxidation
Antioxidant activity, cytotoxic
In-vitro
Terpennoids Endometireal Cancer Cell Induces apoptosis by activation of p53 In-vitro
6-Shogaol Cancer cell Anticancer In-vitro
cells, zerumbone was found to induce glutathione S-
transferase and localize the transcription factor Nrf2, which
binds to the antioxidant response factor gene (ARE) of the
phase II enzyme.25
Zerumbone promotes the expression of several Nrf2/ARE-
dependent phase II enzyme genes, including Y-
glutamyl-cysteine synthetase, glutathione peroxidase, and
hemeoxygenase-1.26 Others have reported that zerumbone
reduces TPA-induced hydrogen peroxide formation and
water retention in proportion to increased levels of
various antioxidant enzymes.26 These types of alterations
were associated with decreased incidence of 7,12-
dimethylbenz[a]anthracene (DMBA)-inducing/promoting
TPA tumors, number of tumors per mouse, and tumor
volume.27
Zerumbone has also been reported to downregulate
CXC chemokine receptor 4 (CXCR4), which is abundantly
expressed in various tumors including breast, ovarian,
prostate, gastrointestinal tract, head and neck, bladder optic
nerve, brain and melanoma.28 Because CXCR4 mediates
the migration of tumor cells to specific organs expressing
its ligand, CXCL12, zerumbone has been suggested as
a potent and potent cancer metastasis inhibitor effective
in blocking CXCR4 in a variety of cancers, including
pancreatic, lung, kidney, and skin cancers.28 In addition,
zerumbone effectively attenuated human mammary gland
tumor cell cytotoxicity and multiple myeloma-induced
osteoclastogenesis and dose-dependently reduced bone
resorption in MDA-bearing Athiorhodaceae nude mice -
MB-231, suggests that it may be effective in preventing
bone cancer-related. bone loss or osteoporosis.6,29 Gingerol
has also been reported to suppress adhesion, invasion,
mobility, matrix metalloproteinase (MMP)-2 and MMP-9
messenger ribonucleic acid (mRNA) expression and protein
activities. in the human breast cancer cell line MDA-MB-
231.30,31
Ginger and its components have been reported to inhibit
tumor promotion in rat skin.32 In particular,16 -gingerol
was found to be highly effective as an anti-skin cancer
agent in vivo in a rat skin model encouraging two-step
initiation. In this model, tumors were initiated with a
single application of DMBA, followed by repeated topical
TPA applications beginning several days later.33 Topical
application of6-gingerol on the shaved backs of female
ICR rats reduces the rate of DMBA-initiated/TPA-promoted
skin papilloma formation and also inhibits epidermal
ornithine decarboxylase activity and inflammation caused
by TPA.34 The results of a similar study indicated that in the
DMBA/TPA skin tumor model, the application of6-paradol
or6-dehydroparadol before TPA application significantly
reduced the number of tumors per mouse. and the number
of mice with tumors.35
Previous studies showed that gingerol was an
effective inhibitor of azoxymethane-induced intestinal
carcinogenesis in rats.36 Ginger supplementation (50 mg/kg
body weight) has been reported to reduce the number of
tumors as well as the incidence of 1,2-dimethylhydrazine
(DMH)-induced colon cancer.37 The effect is attributed
to decreased oxidative damage associated with increased
Nerkar and Ghadge / Current Trends in Pharmacy and Pharmaceutical Chemistry 2022;4(4):158–164 161
activity of catalase, superoxide dismutase, glutathione
peroxidase and glutathione transferase as well as increased
GSH.37 This group then reported that administering
ginger to mice treated with DMH significantly reduced the
incidence and number of tumors as well as the activity of
microbial enzymes (GUSB) and mucopolysaccharidase37
Finally, Wistar rats fed ginger extract (1% dietary blend)
showed a significantly lower number of ureteral lesions
(hyperplasia and neoplasia) compared with the untreated
groups.38
Studies show that compounds in ginger prevent the
proliferation of human cancer cells through the induction
of apoptosis.39,40 A salt extract prepared from ginger
extract suppressed HEp-2 cell proliferation by inducing
cytotoxic effects and DNA fragmentation.41 Ginger extract
and especially6-gingerol were reported to effectively
reduce YYT colonC.10,42 -Gingerol has been reported to
induce a significant and prolonged increase in intracellular
calcium and cytotoxicity in human colorectal cancer SW480
cells.6,43 -Gingerol has been reported to inhibit both
proliferation and infiltration of AH109A ascites cells and
appears to work by inducing S phase arrest, prolonging cell
replication time. of liver tumors and increased apoptosis.44
This compound also induces cell cycle arrest and suppresses
the growth of human pancreatic cancer cell lines, human
pancreatic carcinoma (HPAC) cells, which express wild-
type p53 and BxPC-3 cells expressing a mutant p53
protein.45 Interestingly,6gingerol appeared to be most
effective in inducing apoptosis in p53 mutant cells and
inducing arrest, but not apoptosis in epithelial cells.
present p53.6-Gingerol was further reported to suppress
proliferation and induce apoptosis or G1 cell cycle arrest
in several colorectal cell lines, including HCT116, SW480,
HT29 cells, LoVo and Caco2.46 These effects are associated
with decreased levels of cyclin D1 (a proto-oncoprotein
overexpressed in cancer) and increased expression of the
nonsteroidal anti-inflammatory drug (NSAID) activating
gene (NAG-1), a protein autophagy and antibiotics. 46
Through the comparison of promotion-sensitive (P+)
and promotion-resistant (P-) derivatives of the JB6 mouse
epidermal cell lines, AP-1 was reported to play an
important role in promoting promote tumorigenesis.47
In addition, blocking promoter-induced AP-1 activation
inhibited neoplastic transformation48 Epidermal growth
factor (EGF) is known to induce AP-1 activity and
cell transformation at relatively high levels.47 Previously,
we investigated the effects of two structurally related
compounds from the ginger family,6-gingerol and 6-
paradol, on EGF-induced cellular transformation and
activation. AP.1 chemistry . Our results provided the
first evidence that both compounds block EGF-induced
cellular transformation, but through different mechanisms.6
-Gingerol appears to act by directly inhibiting AP-
1 DNA-binding activity and metabolism, while6-
paradol appears to act by inducing apoptosis49,50 Others
reported that6-gingerol induced DNA fragmentation
and suppressed Bcl-2 expression in HL-60 myeloid
leukemia cells (Wang et al. 2003), and also induced
growth inhibition and caspase-mediated apoptosis in
human squamous cell carcinoma A431 cells.6,51,52 -
paradol and other structurally related derivatives, such
as10 -paradol,3-dehydroparadol, 6-dehydroparadol and 10
-dehydroparadol, inhibited proliferation cells of KB oral
squamous cell carcinoma in record time. and is dose
dependent.6,53 -dehydroparadol was more potent than the
other compounds tested and induced apoptosis by a caspase-
3-dependent mechanism.6,52 -Shogaol [1-(4-hydroxy-3-
methoxyphenyl)-4-lie-3-one], a ketone from ginger, exhibits
the strongest cytotoxicity against humans A549, SK-OV -
3, SK-MEL-2, and HCT15 tumor cells, compared with4-
,6-,8,- and10 –gingerroot.54 This compound also inhibited
the proliferation of several transgenic mouse ovarian cancer
cell lines, including C1 and C2.54 In addition,6-shogaol
has been reported to inhibit growth and induce apoptosis
in COLO 205 cells.55 Treatment with6-shogaol, but not 6
-gingerol, induces DNA fragmentation in COLO 205 colon
cancer cells. Death is mediated by activation of caspase-9,
- 3 and -8, leading to mitochondrial cytochrome c release,
modulation of pro-apoptotic Bax and negative effects of
anti-apoptotic Bcl2, and induction of growth arrest and
DNA damage (GADD)-factor transcribed 153 (GADD153)
mRNA and protein.55
NF-κB is a rapidly induced stress-responsive
transcription factor that enhances the transcription of
many genes, including cytokines, growth factors, and
acute-responsive proteins.56 Its activation is also implicated
in the mitogen-activated protein (MAP) kinase signaling
pathways.57 The mechanism of NF-κB activation is well
known. In its inactive form, NF-κB found in the cytosol
binds to an inhibitory protein known as kappa inhibitor
B (IκB). When stimulated, IκB is phosphorylated by an
IκB kinase, releasing it from NF-κB and subsequently
degraded. After detaching from IκB, NF-κB is transferred
to the nuclear region, where it activates gene transcription
by binding to its specific DNA sequence present in certain
genes. Importantly, NF-B activation has been implicated
in the initiation or acceleration of tumorigenesis,58 and in
JB6 cells, NF-κB inhibition also suppresses tumorigenesis.
cell changes induced by tumor promoters (60, Li et al.
1997).6-Gingerol may exert its effects by blocking the
NF-κB/COX-2 pathway. This idea is supported by data
indicating that the reduction of UVB-induced expression
and COX-2 metabolism by6-gingerol is associated with
inhibition of IκBα(Ser32) phosphorylation leading to
to reduce NF-κB translocation from the cytosol to the
nucleus in HaCaT cells.59 A ginger extract given to mice
with experimentally induced liver cancer reduced NF-κB
and TNF-α.6,60 -Gingerol has been reported to block
162 Nerkar and Ghadge / Current Trends in Pharmacy and Pharmaceutical Chemistry 2022;4(4):158–164
TNF-linked apoptosis.
Zerumbone has been reported to block NF-κB activation
induced by a variety of stimuli, including tumor necrosis
factor (TNF), cigarette smoke condensation, and hydrogen
peroxide.61 It also blocks phosphorylation and degradation
of IκBαkinase, leading to downregulation of constitutively
active NF-κB and some of its upregulated gene targets,
such as COX-2, cyclin D1, Bcl2. and anti-apoptotic genes,
thereby enhancing chemotherapy-induced cell death.62
Zerumbone has also been reported to block the activity of
the NF-κB ligand receptor activator (RANKL) in mouse
monocytes (progenitor cells of osteoclasts) by inhibiting the
activity, phosphorylation and degradation of kinase IκBα
(Sung et al. 2009). Oral administration of zerumbone (100,
250, or 500 ppm) to ICR mice reduces the inflammation
and diversity of colon adenocarcinoma induced by
intraperitoneal injection of azoxymethane (AOM, 10 mg/kg
body weight; Kim et al. 2009). In addition, zerumbone (250
or 500 ppm) effectively suppressed 4-(methylnitrosamino)-
1-(3-pyridyl)-1-butanone-induced lung adenoma formation
in female A/J mice.52 This ginger derivative appears to
exert its effects through inhibiting proliferation, inducing
apoptosis, and inhibiting the expression of NF-B and
heme oxygenase in colon cancer tissues. and lungs63 In a
previous study, 6-gingerol was reported to be able to inhibit
both vascular endothelial growth factor (VEGF) and basic
fibroblast growth factor (bFGF) inducing proliferation.
human endothelial cells and induce cell cycle arrest in
the G1 phase.6,64 -Gingerol also suppresses capillary-
like tubule formation by endothelial cells in response to
vascular endothelial growth factor (VEGF), and strongly
inhibits endothelial cell germination. in the rat aorta and the
formation of new blood vessels in the rat cornea in response
to VEGF.65
Researchers have suggested that the effectiveness of
ginger may be related to its ability to inhibit prostaglandin
and leukotriene biosynthesis.66 Some researchers have
shown that gingerol actively inhibits arachidonate 5-
lipoxygenase, an enzyme in leukotriene biosynthesis67 The
protein leukotriene A4 hydrolase (LTA4H) was considered
a suitable target for cancer therapy and our prediction in
silico using reverse splicing suggested that LTA4H could
be a potential target for6– gingerol.68 The prediction
is supported by the study that6-gingerol suppresses the
growth of cancer cells independent of the anchorage by
binding to LTA4H and inhibiting the activity of LTA4H
in HCT116 colorectal cancer cells. It was also found
that6-gingerol effectively suppressed tumor growth in
vivo in nude mice, an effect mediated by inhibition of
LTA4H activity. Taken together, these results point to an
important role for LTA4H in cancer and also support
the antitumor efficacy of6-gingerol targeting LTA4H in
preventing colorectal cancer. 68 More importantly, these are
the first results to identify a direct target of6-gingerol to
explain its antitumor activity. 69
It was found that when cultured ovarian cancer cells
were treated with6-shogaol, they exhibited marked
inhibition associated with NF-κB inhibition as well as
inhibition angiogenic factors, VEGF and IL-8. Therefore,
this compound plays an active role in preventing cancer
angiogenesis.70 Furthermore, it was concluded that people
consuming dietary ginger (0.5% or 1.0%) showed no
activity on malformation of aberrant crypt foci formation
(ACF). or decreased proliferation index or crypt cells of
the apoptotic colon induced by DMH. in DMH-treated rats.
Furthermore, as demonstrated,70,71 ginger extract could
not inhibit the growth of N-butyl-N-(4-hydroxybutyl)-
nitrosamine (BBN)/N-methyl- N-nitrosourea (MNU)-
induced bladder cancer in male Swiss rats and in mice
treated with BBN/MNU/2% ginger, the incidence of grade
2 translocation cell carcinoma was increased.72
3. Conclusion
Ginger and its active components inhibit growth and
proliferation of many cancer cells. Also 6-gingerol and
other active constituents in ginger inhibited the growth of
many cell-lines and showed cyto-toxic properties. Thus, the
anticancer properties of ginger described in this review may
give a new direction for anticancer drug discovery.
4. Source of Funding
AGN for funding this project through Ateos Foundation of
Science Education and Research, Pune, M.S., India
5. Conflict of Interest
None.
6. Acknowledgement
The Author SG thanks AGN for funding this project through
Ateos Foundation of Science Education and Research,
Pune, M.S., India, also waiver for the publications and
acknowledges the same.
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Author biography
Amit Gajanan Nerkar, Professor and Research Head
https://orcid.org/0000-0002-1377-8466
Srushti Ghadge, Student
Cite this article: Nerkar AG, Ghadge S. Ethnopharmacological review
of ginger for anticancer activity. Curr Trends Pharm Pharm Chem
2022;4(4):158-164.
