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Document heading doi:10.12980/JCLM.2.2014J10 襃 2014 by the Journal of Coastal Life Medicine. All rights reserved.
Evaluation of anti-inflammatory potential of Nardostachys jatamansi
rhizome in experimental rodents
Rajnish Kumar Singh1, Vaishali1, Susanta Kumar Panda2, Padala Narasimha Murthy2, Ghanashyam Panigrahi2, Pramod Kumar
Sharma3, Ramesh Kumar Gupta1,2*
1Moradabad Educational Trust, Group of Institution Faculty of Pharmacy, Moradabad-244001, Uttar Pradesh, India
2Royal College of Pharmacy and Health Sciences, Berhampur-760002, Orissa, India
3School of Medical & Allied Sciences, Galgotias University, G.B. Nagar-201306, Uttar Pradesh, India
Journal of Coastal Life Medicine 2014; 2(1): 38-43
Journal of Coastal Life Medicine
*Corresponding author: Ramesh Kr. Gupta, Moradabad Educational Trust, Group of
Institution Faculty of Pharmacy, Moradabad-244001, Uttar Pradesh, India.
Tel: +91 9451529612
Fax: +91 591 245221
E-mail: ram5880@gmail.com
Foundation Project: Supported by Royal College of Pharmacy and Health Sciences
Berhampur (Grant No-RCPHS/PH-09).
1. Introduction
Pain is a common symptom of various inflammatory
diseases and is the primary reason why patients pursue
specialised treatment[1]. Thus, there is a great demand for
more effective anti-inflammatory drugs[2]. Because currently
available anti-inflammatory drugs have considerable
side effects that inhibit their clinical use, many studies
are currently underway to develop new treatments for
inflammatory diseases[3]. The search for alternatives to
current treatments is necessary and will greatly benefit
those afflicted with inflammatory diseases[4]. Natural
products have been one of the most successful sources for
the discovery of new therapeutic agents[5]. Nardostachys
jatamansi (N. jatamansi, commonly named as jatamansi)
belongs to family Valerianaceae.
N. jatamansi is perennial herb whose rhizome and roots
are mainly used as drug. N. jatamansi is described in
PEE R REVIEW ABSTR ACT
KEYWORDS
Nardostachys jatamansi rhizome, Anti-inflammatory, Histamine, Carrageenin, Cotton pellet
granuloma
Objective: To evaluate the anti-inflammatory effect of Nardostachys jatamansi (N. jatamansi)
rhizome against acute, subacute and chronic models of inflammation in experimental animals.
Methods: N. jatamansi rhizome extract (150 and 300 mg/kg, p.o.) and the reference drugs
phenylbutazone (100 mg/kg, p.o.) and acetylsalicylic acid (300 mg/kg, p.o.) were evaluated using
models for inflammation (autacoids induced hind paw oedema, formaldehyde induced hind paw
oedema, carrageenin-induced paw oedema, cotton pellet granuloma and subcutaneous air pouch
model).
Results: In acute inflammation as produced by carrageenin 29.06% and 55.81%, by histamine
25.0% and 39 .28%, by 5-hydroxytryptamine 21.37% and 36.95% and by prostaglandin E2-
induced hind paw oedema 31.03% and 44.82% protection was observed. While in subacute anti-
inflammatory models using formaldehyde-induced hind paw oedema (after 1.5 h) 13.88% and
33.33% and in chronic anti-inflammatory model using cotton pellet granuloma 7.4% and 17.58%
protection from inflammation was observed. N. jatamansi rhizome extract also inhibited the
inflammatory mediators (nitric oxide by 12.81% and 38.41%, by prostaglandin E2 12.58% and 47.82%
while by TNF-α 13.51% and 41.89%) produced in the pouch.
Conclusions: The results of this study strongly indicate the protective effect of N. jatamansi
rhizome extract against acute, subacute and chronic models of inflammation, which may be
attributed to its anti-inflammatory potential.
Peer reviewer
Prof. (Dr.) Sudhansu Ranjan Swain,
Sherwood Co l l e g e of Pharmacy,
Barabanki, Uttar Pradesh, India.
Tel: +91 9412391802
Fax: +91 0522 2716698
E-mail: sudhansu2004@gmail.com
Comments
This is a valuable research work in
which authors have demonstrated
the anti-inflammatory potential of N.
jatamansi rhizome in experimental
rodents. The activity was assessed
based on inflammatory mediators
which are the prime sign of
inflammation. NJE was found to be
a promising an anti-inflammatory
activity against acute, subacute and
chronic model induced inflammation.
Details on Page 42
Article history:
Received 23 Dec 2013
Received in revised form 1 Jan, 2nd revised form 7 Jan, 3rd revised form 13 Jan 2014
Accepted 22 Jan 2014
Available online 28 Jan 2014
journal homepage: www.jclmm.com
Rajnish Kumar Singh et al./Journal of Coastal Life Medicine 2014; 2(1): 38-43 39
Indian traditional system of medicine (Ayurveda) for its use
in mental disorders, insomnia, hyperlipademia, hypertension
and heart diseases and memory improvement[6,7]. It has
protective effect in Parkinsonism, epilepsy, cerebral
ischemia and free radical scavenging activity[8]. Jatamansi
showed antifungal, antioestrogenic, and jatamansone has
been reported to possess anti-arrythmatic, anti-asthmatic,
nematicidal and anti-bacterial activity[9]. Jatamansi is
capable of lowering norepinephrine as well as serotonin in
brain[10]. To the best of our knowledge, there has been not
any research reported on anti-inflammatory activity on N.
jatamansi. Therefore, the present study was designed to
demonstrate the anti-inflammatory effect of N. jatamansi
extract (NJE) in experimental animals.
2. Materials and methods
2.1. Chemicals
Carrageenin, histamine, 5-hydroxytryptamine (5-HT),
prostaglandin E2 (PGE2), bradykinin, acetylsalicylic acid
(ASA) and phenylbutazone (PBZ) were purchased from Sigma
Chemicals and formaldehyde from British Drug House,
Mumbai, India. All the chemicals used were of analytical
grade.
2.2. Animals
Wistar rats weighing 200-250 g of either sex were procured
from Royal college of Pharmacy, Health and Sciences
Berhampur, Orissa. They were kept in departmental animal
house in well cross ventilated room at (22依2) °C with light
and dark cycles of 12 h for 1 week before and during the
experiments. All studies were performed in accordance
with the guide for the care and use of laboratory animals, as
adopted and promulgated by the Institutional Animal Care
Committee, CPCSEA, India (Reg. No. 1018C/06/CPCSEA).
2.3. Preparation of plant extract
The plant material (dried rhizome) was procured from local
market of Berhampur, Orissa, India in December 2010. The
plant material was identified and the voucher specimen was
deposited in the institutional herbarium. The rhizomes of
plants of N. jatamansi were washed thoroughly in tap water,
shade dried and powdered. Crushed material was subjected
to extraction in a Soxhlet apparatus at 60-70 °C for 6 h
continuously in 50% distilled ethanol. The extracted material
was evaporated to dryness under reduced pressure (40-45
°C). The yield of the material was 14.65%. This crude extract
was referred to as NJE. The extract obtained was further
subjected to pharmacological investigation.
2.4. Anti-inflammatory activity
2.4.1. Study of NJE on acute inflammation
2.4.1.1. Carrageenin-induced hind paw oedema in rats
The acute hind paw oedema was produced by injecting
0.1 mL of carrageenin (prepared as 1% suspension in 1%
carboxymethyl cellulose) locally into the plantar aponeurosis
of the right hind paw of rats[11]. NJE (150 and 300 mg/kg, p.o.)
was administered to two different groups while the other two
groups served as negative and positive controls and received
vehicle (1 mL/kg, p.o.) and standard drug, acetylsalicylic
acid (ASA, 300 mg/kg, p.o.), respectively. NJE and ASA were
administered 1 h prior to the injection of carrageenin. The
rat pedal volume up to the ankle joint was measured using
plethysmometer (Ugo Basile, 7140 Comerio-varese, Italy) at
0 h (just before) and 3 h after the injection of carrageenin.
Increase in the paw edema volume was considered as the
difference between 0 and 3 h. Percent inhibition of oedema
volume between treated and control groups was calculated
as follows:
Percent inhibition=(1-Vt/Vc)伊100
Where Vc and Vt represent the mean increase in paw
volume in control and treated groups, respectively.
2.4.1.2. Autacoids-induced hind paw oedema in rats
This experiment was conducted as per the methodology
used by Singh and Pandey[12]. The autacoids, viz., histamine
(1 mg/mL), 5-HT (1 mg/mL), PGE2 (1 µg/mL) and bradykinin
(20 µg/mL) were employed as phlogistic agents. The effect of
NJE (150 and 300 mg/kg, p.o.) was tested individually against
each autacoid. Right hind paw oedema was induced by the
sub-plantar injection of 0.1 mL of respective phlogistic
agent. Test compounds were administered 1 h prior to the
inflammatory insult. The pedal volume was measured just
before (0 h) and 3 h after the phlogistic challenge. PBZ (100
mg/kg, p.o.) was employed as reference standard.
2.4.2. Study of NJE on subacute inflammation
2.4.2.1. Formaldehyde-induced hind paw volume
The test was performed according to the technique
developed by Brownlee[13]. Pedal inflammation was induced
by injecting 0.1 mL of 4% formaldehyde solution below the
plantar aponeurosis of the right hind paw of the rats. The
paw volume was recorded immediately prior to compound
administration (0 h) and then at 1.5, 24 and 4 8 h after
formaldehyde injection. Vehicle (1 mL/kg, p.o.), NJE (150 and
300 mg/kg, p.o.) and standard drug, ASA (300 mg/kg, p.o.) were
administered 1 h prior to formaldehyde injection.
2.4.3. Study of NJE on chronic inflammation
2.4.3.1. Cotton pellet granuloma in rats
The effect of NJE on chronic or proliferative phase of
inflammation was assessed in cotton pellet granuloma rat
model as described by Winter and Porter[14]. Autoclaved
cotton pellets weighing (35依1) mg each were implanted
subcutaneously through small incision made along the
axilla or flank region of the rats anesthetized with ether.
The different groups of rats were administered the NJE (150
and 300 mg/kg, p.o.) and ASA (300 mg/kg, p.o.) once daily for
7 consecutive days from the day of cotton pellet insertion.
The control group received vehicle (1 mL/kg, p.o.). On the
eighth day, all the rats were sacrificed and the cotton pellets
covered by the granulomatous tissue were excised and dried
in hot air oven at 60 °C till a constant weight was achieved.
Rajnish Kumar Singh et al./Journal of Coastal Life Medicine 2014; 2(1): 38-43
40
Granuloma weight was obtained by subtracting the weight
of cotton pellet on 0 d (before start of experiment) from the
weight of the cotton pellet on eighth day.
2.4.3.2. Subcutaneous air pouch (SAP)
The SAP protocol used was similar to that described by
Raymundo et al[15]. Briefly, air pouches were produced
by subcutaneous injections of 10 mL of sterile air into the
intrascapular region of the mice. After 3 d, another 10 mL of
air was injected to maintain the pouches. Three days after
this last injection, animals received an injection of 0.5 mL of
sterile carrageenan suspension (1%). Mice were pre-treated
with oral doses of vehicle, dexamethasone (0.5 mg/kg) and
NJE 1 h before and 23 h after carrageenan injections in the
SAP. Animals were sacrificed 24 h after the carrageenan
injection, and the cavity was washed with 2mL of sterile
phosphate buffer. Exudates were collected. An aliquot of
exudates was diluted 1:20 in Turk liquid (0.5% crystal violet
dissolved in 30% acetic acid). The exudates were centrifuged
at 4 000 r/min for 10 min at 4 °C; the supernatants were
collected and stored at -20 °C until further analysis.
2.4.3.2.1. TNF-α and PGE2 measurements
Supernatants from exudates collected in the SAP were used
to measure, TNF-α, and PGE2. TNF-α were quantified by
enzyme-linked immunosorbent assay, using the protocol
supplied by the manufacturer (Peprotech). PGE2 was
determined by using EIA kits (Cayman Chemical Co., MI, USA),
according to the method of Pradelles et al[16].
2.4.3.2.2. Nitrate measurement
To evaluate NO production, nitrate (the stable metabolite
of NO) concentration in the supernatants was measured
according to Xu et al.[17] with several modifications[15]. The
absorbance was measured at 540 nm using amicroplate
reader, and the nitrate concentration was calculated using a
standard curve of sodium nitrate.
2.5. Statistical analysis
The values were represented as mean依SEM for six animals.
Analysis of variance test was followed by individual
comparison by Newman-Keuls test using Prism Pad software
(Version 3.0) for the determination of level of significance.
The value of P<0.05 was considered statistically significant.
3. Results
3.1. Effect of NJE on carrageenin-induced hind paw oedema
The mean increase in paw oedema volume was about (0.86依
0.11) mL in the vehicle-treated control rats. NJE (150 and 300 mg/
kg, p.o.) significantly reduced the mean paw oedema volume
at 3 h after carrageenin injection. NJE (150 and 300 mg/kg, p.o.)
exhibited anti-inflammatory activity in a dose-dependent
manner with the percent inhibition of paw oedema of 29.06
and 55.81 respectively, as compared with the control group.
However, the standard drug, ASA (300 mg/kg, p.o.) showed highly
significant (P<0.001) anti-inflammatory activity with the percent
inhibition of 69.76 (Table 1).
Table 1
Effect of NJE on carrageenin induced hind paw oedema and cotton
pellet granuloma in rats.
Drug Dose
(mg/kg)
Carrageenin-induced
paw oedema volume
(mL)
%
Protection
Weight of cotton
Pellet granuloma
(mg)
%
Protection
Control - 0.86依0.11 -106.15依2.50 -
ASA 300 0.26依0.03c69.76 67.28依1.85c36.61
NJE 150 0.61依0.08a29.06 98.21依2.10a 7.40
NJE 300 0.38依0.05b55.81 87.48依2.00c17.58
Values are mean依SEM of 6 rats in each group.
a: P<0.05, b: P<0.01, c: P<0.001 compared with control group.
3.2. Effect of NJE on cotton pellet granuloma
The study of NJE on proliferative phase of inflammation
indicated that NJE (150 and 300 mg/kg, p.o.) significantly (P<0.05;
P<0.001) reduced the granuloma formation with inhibition of
7.4% and 17.58% as compared with ASA (300 mg/kg, p.o.), which
showed significant (P<0.001) inhibition on granuloma formation
with the percent inhibition of 36.61 (Table 1).
3.3. Effect of NJE on autacoids-induced hind paw oedema
The mean increase in paw oedema volume produced at 3
h after injection of different autacoids, viz., histamine, 5-HT,
PGE2 and bradykinin was (0.28依0.02), (0.46依0.04), (0.29依0.04)
and (0.28依0.04) mL, respectively. NJE (150 and 300 mg/kg, p.o.)
significantly inhibited hind paw oedema induced by histamine
(25%, P<0.01 and 39.28%, P<0.001), 5-HT (21.37%, P<0.05 and
36.95%, P<0.001) and PGE2 (31.03%, P<0.05 and 44.82, P<0.001)
respectively, but not that of bradykinin. However, PBZ (100 mg/
kg, p.o.) significantly (P<0.001) inhibited all autacoids including
bradykinin induced hind paw oedema with 53.57, 54.34, 62.06
and 42.85 percent inhibition (Table 2).
3.4. Effect of NJE on formaldehyde-induced hind paw oedema
Table 2
Effect of NJE on autacoids induced hind paw oedema in rats.
Drug Dose
(mg/kg)
Histamine 5-HT PGE2Bradykinin
Increase in oedemar
volume (mL)
% Protection Increase in oedemar
volume (mL)
% Protection Increase in oedemar
volume (mL)
% Protection
Control - 0.28依0.02 -0.46依0.02 -0.29依0.04 -0.28依0.04
PBZ 100 0.13依0.01c53.57 0.21依0.01c54.34 0.11依0.01c62.06 0.16依0.02c
NJE 150 0.21依0.02b25.00 0.36依0.03a21.37 0.20依0.02a31.03 0.26依0.02
NJE 300 0.17依0.01c39.28 0.29依0.02c36.95 0.16依0.03b44.82 0.27依0.03
Values are mean依SEM of 6 rats in each group.
a: P<0.05, b: P<0.01, c: P<0.001 compared with control group.
Rajnish Kumar Singh et al./Journal of Coastal Life Medicine 2014; 2(1): 38-43 41
NJE (150 mg/kg, p.o.) significantly diminished the mean
paw oedema volume at 1.5 h (13.88%) (P<0.05) and 24 h (5.43%)
(non significant). The maximum inhibition of oedema volume
produced by NJE (300 mg/kg, p.o.) was almost comparable to
that of ASA (300 mg/kg, p.o.) (51.38% versus 55.55% at 1.5 h).
Interestingly, the effect of NJE persisted up to a period of 24 h
in contrast to ASA, the effect of which was significant only at
1.5 h (Table 3).
Table 3
Effect of NJE on formaldehyde induced hind paw oedema in rats.
Drug Dose
(mg/kg)
Formaldehyde induced hind paw oedema volume (mL)
1.5 h %
Protection 24 h %
Protection 48 h %Protection
Control - 0.72依0.04 -0.92依0.07 -0.51依0.06 -
ASA 300 0.32依0.02c55.55 0.54依0.03c41.30 0.49依0.05 3.92
NJE 150 0.62依0.03a13.88 0.87依0.06 5.43 0.48依0.04 5.80
NJE 300 0.35依0.04c51.38 0.71依0.05a22.82 0.47依0.03 7.80
Values are mean依SEM of 6 rats in each group.
a: P<0.05, b: P<0.01, c: P<0.001 compared with control group.
3.5. Effect of NJE on TNF-α, nitric oxide and PGE2
This inflammatory response was also accompanied by
an increase in the levels of TNF-α (496.11%), nitric oxide
(312.33%),) and PGE2 (132.46%) were observed in the vehicle-
treated group when compared with PBS. Pre-treatment of
mice with NJE significantly suppressed the carrageenan-
induced NO, PGE2 and TNF-α level in the vehicle-treated
group when compared with PBS. NJE (150 mg/kg, p.o.)
exhibited anti-inflammatory response in a dose-dependent
manner with the percent inhibition of the level of TNF-α,
NO and PGE2 as 13.15, 12.81 and 12.58 respectively. While
the inhibition of percentage produced by NJE (300 mg/
kg, p.o.) in TNF-α, NO and PGE2 as 41.89, 38.41 and 47.82
respectively. However, ASA (300 mg/kg, p.o.) significantly
(P<0.001) inhibited TNF-α (66.57%), nitric oxide (81.4%) and
PGE2 (61.69%). That means the ASA showed the maximum
percentage inhibition as compared to vehicle treated group
(Table 4).
Table 4
Effect of NJE on NO (µmol/L), PGE2 (pg/mL) and TNF-α (ng/mL)
production in the SAP model.
Drug Dose NO (µmol/L)PGE2 (pg/mL)TNF-α (ng/mL)
Vehicle - 67.21依2.40 89.71依3.40 79.82依2.38
PBS 100 16.30依0.81† 38.59依1.80† 3.39依0.98†
NJE 150 58.60依2.10b 78.42依2.60b 69.32依2.20b
NJE 300 41.39依2.00c 46.81依2.20c 46.38依2.60c
ASA 300 12.51依0.96c 34.37依2.10c 26.68依2.10c
Values are mean依SEM of 6 rats in each group.
†: P<0.001 compared with vehicle-treated mice with the PBS-treated
group; a: P<0.05, b: P<0.01, c: P<0.001 compared with Vehicle treated
group.
4. Discussion
The present study demonstrates the potent anti-
inflammatory activity of the ethanolic extract of N .
jatamansi rhizome in different models of inflammation,
i.e., acute exudative (carrageenin-induced rat paw
oedema), subacute (formaldehyde) and chronic proliferative
inflammation (cotton pellet granuloma), there by indicating
the possibility of developing N. jatamansi rhizome as the
cheaper, safer and potent anti-inflammatory therapeutic
agent. Carrageenan is the phlogistic agent of choice for
testing anti-inflammatory drugs as it is not known to be
antigenic and is devoid of apparent systemic effects[18]. The
carrageenin induced paw oedema model in rats is known to
be sensitive to cycloxygenase inhibitors and has been used
to evaluate the effect of non-steroidal anti-inflammatory
agents[19]. The oedema and inflammation induced by
carrageenin is shown to be mediated by histamine and 5-HT
during first 1 h. After which increased vascular permeability
is maintained by the release of kinins up to 2.3 h and from
2.3 to 6.0 h, the mediators appear to be prostaglandins,
the release of which is closely associated with migration
of leucocytes into the inflamed site[20]. It is well known
that carrageenan induced paw oedema is characterized by
biphasic event with involvement of different inflammatory
mediators. In the first phase (during the first 2 h after
carrageenan injection), chemical mediators such as
histamine and serotonin play role, while in second phase
(3-4 h after carrageenan injection) kinins and prostaglandins
are involved[21].
Our results revealed that administration of ethanolic
extract of N. jatamansi inhibited the oedema starting
from the first hour and during all phases of inflammation,
which is probably inhibition of different aspects and
chemical mediators of inflammation. In autacoids induced
inflammations, N. jatamansi produced significant inhibitory
activity against histamine, 5-HT and PGE2 induced hind
paw oedema in rats but failed to exhibit activity against
bradykinin induced hind paw oedema. Administration of
N. jatamansi at different doses level (150 and 300 mg/kg)
attenuated the increased pedal volume against the phlogistic
challenge. N. jatamansi caused a subsequent recovery
towards normalization comparable to the PBZ group animals.
Inflammation induced by formaldehyde is biphasic, an
early neurogenic component is mediated by substance P
and bradykinin followed by a tissue mediated response
where histamine, 5-HT and bradykinin are known to be
involved[22]. In the formaldehyde-induced inflammation, the
N. jatamansi demonstrated significant anti-inflammatory
activity that lasted up to 24 h in contrast to ASA, which
was effective only at 1.5 h, suggesting its long duration
of action. The cotton-pellet granuloma is widely used to
evaluate the transudative and proliferative components of
the chronic inflammation[23]. In order to assess its efficacy
against proliferative phase of inflammation in which
tissue degeneration and fibrosis occur, the widely used
cotton pellet granuloma test was employed. During the
repair process of inflammation, there is proliferation of
macrophages, neutrophils, fibroblasts and multiplication of
small blood vessels, which are the basic sources of forming
a highly vascularised reddish mass, termed granulation
tissue[24,25]. Though N. jatamansi (150 and 300 mg/kg, p.o.)
significantly reduced the granuloma formation, the effect
was of less intensity, when compared with ASA (300 mg/
kg, p.o.). Macrophages are the first line of defence against
microbial invaders and malignancies by nature of their
Rajnish Kumar Singh et al./Journal of Coastal Life Medicine 2014; 2(1): 38-43
42
phagocytic, cytotoxic and intracellular killing capacities[26].
Macrophage activation by lipopolysaccharide results in the
release of several inflammatory mediators such as NO and
the proinflammatory cytokines, TNF-α[27]. NO is a highly
reactive molecule produced from guanidine nitrogen of NO
synthase.
However, overproduction of NO can be harmful and may
result in septic shock, neurologic disorders, rheumatoid
arthritis, and autoimmune diseases[28]. Therefore, inhibition
of NO production is an important therapeutic target in the
development of anti-inflammatory agents. In this study,
we demonstrated that the ethanolic extract of N. jatamansi
suppressed NO production and TNF-α secretion at higher
doses, both of which are crucial in the inflammatory and
healing mechanism and naturally occurring flavonoids,
such as rutin and quercetin, have been reported to scavenge
NO[29]. It is well known that PGE2 is factors involved in
many inflammatory processes[30] and in pain induction and
perception[31]. PGE2 increases in parallel with tissue oedema,
a condition which can be suppressed by NSAIDs (inhibitors
of cycloxygenase)[32].
The increase in TNF levels in the SAP were accompanied by
a corresponding increase in interferon. Significant increase
in the level of TNF, a cytokine that plays an important role
in acute phase reactions and immune response[33], was
observed. NJE also inhibited PGE2 and TNF production.
As seen in this experiment, the ability of this extract to
suppress inflammation when it is applied after the onset
of inflammation is likely to be due to the genuine anti-
inflammatory activity.
Conflict of interest statement
We declare that we have no conflict of interest.
Acknowledgements
The authors are thankful to the Director of Royal college
of Pharmacy and Health Sciences, Berhampur, Orissa and
Moradabad Educational Trust Group of Institution Faculty
of Pharmacy, Moradabad, for providing necessary facilities
throughout this research. The entire grants were provided by
Royal College of Pharmacy and Health Sciences Berhampur
(Grant No-RCPHS/PH-09).
Comments
Background
The research into plants with alleged folkloric use as anti-
inflammatory agents should therefore be viewed as a fruitful
and logical research strategy in the search for new anti-
inflammatory drugs. The inflammatory response involves a
complex array of enzyme activation, mediator release, fluid
extravasations, cell migration, tissue breakdown and repair
which are aimed at host defense and usually activated
in most disease condition. Currently much interest have
been paid in the searching of medicinal plants with anti-
inflammatory activity which may lead to the discovery of
new therapeutic agent that is not only used to suppress the
inflammation but also used in diverse disease conditions
where the inflammation response in amplifying the disease
process. There is a growing interest in herbal remedies
because of their effectiveness, minimal side effects in
clinical experience and relatively low cost. Therefore,
present study was designed to demonstrate the evaluation
of anti-inflammatory potential of N. jatamansi rhizome in
experimental rodents.
Research frontiers
The inflammation is the common health problems in the
recent therapeutic scenario. Mostly the drugs from natural
origin are widely used as an anti-inflammatory agent,
which is caused by biological and chemical agent. While
screening of ethanolic extract of N. jatamansi rhizome
showing significant anti-inflammatory activity against
acute, subacute and chronic induced inflammation.
Related reports
The objective of this study, to assess the anti-
inflammatory activity of N. jatamansi rhizome against acute,
subacute and chronic induced inflammation. NJE ( 150 and
300 mg/kg, p.o.) and the reference drugs phenylbutazone
(PBZ: 100 mg/kg, p.o.) and ASA ( 300 mg/kg, p.o.) were
evaluated using different models for inflammation. In
subacute anti-inflammatory models using formaldehyde-
induced hind paw oedema, in chronic anti-inflammatory
model using cotton pellet granuloma. The folklore medicine
has evidence of effectiveness of herbs in treating various
types of inflammation.
Innovations and breakthroughs
N. jatamansi (commonly known as jatamansi), is a
medicinal plant used in various Ayurvedic formulations.
In the present study, authors have demonstrated the
anti-inflammatory activity of N. jatamansi rhizome in
experimental animals. From the results, it is clear that the
NJE has shown dose dependent activity among which at the
dose level of 300 mg/kg, p.o. shows greater activity which is
comparable with the control and standard groups.
Applications
The treatment with NJE significantly prevents the drug
induced inflammation. As seen in this experiment, the
ability of this extract to suppress inflammation when it is
applied after the onset of inflammation is likely to be due to
the genuine anti-inflammatory activity. From the literature
survey, it has been found that N. jatamansi is safe to
humans. Thus, NJE is use for the treatment of inflammation.
Peer review
This is a valuable research work in which authors
have demonstrated the anti-inflammatory potential of N.
jatamansi rhizome in experimental rodents. The activity was
assessed based on inflammatory mediators which are the
prime sign of inflammation. NJE was found to be a promising
an anti-inflammatory activity against acute, subacute and
chronic model induced inflammation.
Rajnish Kumar Singh et al./Journal of Coastal Life Medicine 2014; 2(1): 38-43 43
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