Ulcerogenic Effect

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ANTI-ULCEROGENIC EFFECT OF MORINDA CITRIFOLIA IN VARIOUS EXPERIMENTAL MODELS

ANTI-ULCEROGENIC EFFECT OF MORINDA CITRIFOLIA IN VARIOUS EXPERIMENTAL MODELS

To further confirm its anti-ulcerogenic effect ethanol extract was evaluated for Cold-restraint stress - induced ulcer model. Gastric ulceration induced by stress is probably mediated by the presence of acid, increase in gastric motility, [25] mast cell degranulation[26], decreased gastric mucosal blood flow [27], decreased prostaglandin synthesis [28] and augmented excretion of glycoproteins in the mucus [29]. Moreover, stress-induced ulcer can be prevented partially or entirely by vagotomy; vagal over activity has been suggested to be the principal factor in stress-induced ulceration [30]. Any of these factors could play a role in genesis of stress-induced ulcers. Oral administration of the ethanolic extracts of Morinda citrifolia showed dose dependent inhibition of gastric ulceration induced by Cold-restraint stress.
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Design, Characterization and Anti-ulcerogenic Effect of Amoxicillin trihydrate Thiolated Chitosan Mucoadhesive Microspheres for Effective Treatment of H. pylori

Design, Characterization and Anti-ulcerogenic Effect of Amoxicillin trihydrate Thiolated Chitosan Mucoadhesive Microspheres for Effective Treatment of H. pylori

Amoxicillin (α-amino-hydroxybenzylpenicillin) is a semi-synthetic, orally absorbed, broad-spectrum antibiotic. It is now widely used in the standard eradication treatment of gastric and duodenal ulcers, which are associated with H. pylori infection combined with a second antibiotic and an acid-suppressing agent. The aim of this study was to develop controlled release mucoadhesive microspheres of amoxicillin trihydrate for the treatment of gastric and duodenal ulcers caused by Helicobacter pylori (H. pylori) and evaluated anti-ulcerogenic effect of microsphere. Amoxicillin loaded thiolated chitosan microspheres were prepared by emulsifying method using liquid paraffin light and heavy in ratio of 50:50 as a dispersing medium and glutaraldehyde used as a cross-linking agent. The prepared microspheres were evaluated for mean particle size and particle size distribution, shape and surface morphology, drug content, mucoadhesion measurement and in-vitro drug release. FT-IR spectroscopic analysis was performed to ascertain drug polymer interaction. Antiulcer activity of amoxicillin microspheres was investigated on Indomethacin induced gastric ulcer model in Albino rats. The antiulcer capability of amoxicillin microspheres was compared to 100mg/kg cimetidine. Gastric ulcers were induced in Wistar albino rats by oral administration of indomethacin (5 mg/kg), antiulcer activity of amoxicillin microspheres (100, 200mg/kg, p.o) was observed on ulcer index and gastric pH. Statistical analysis was done by One-way ANOVA followed by Tukey’s post hoc test. The release profiles showed Korsmeyer-Peppas release behavior up to 48 hours where the highest drug release was 76.7±3.52% of the amoxicillin loaded in the thiolated chitosan microspheres, indicating a strong crosslinking between chitosan and glutaraldehyde. Amoxicillin microspheres produced significant (P<0.05) decrease in ulcer index and gastric pH as compared to control. The anti-ulcer effects of amoxicillin microspheres were dose dependent manner. From the results of the present investigation it may be concluded that drug loaded chitosan microspheres can be prepared by a simple technique which avoids the use of complex apparatus and special precautions and microsphere produced significant anti-ulcer effects in experimental models.
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A PRE CLINICAL COMPARATIVE STUDY OF THE ANTI GASTRIC ACID SECRETORY AND ANTI ULCEROGENIC EFFECT OF ROXATIDINE AND RABEPRAZOLE USING A RAT MODEL

A PRE CLINICAL COMPARATIVE STUDY OF THE ANTI GASTRIC ACID SECRETORY AND ANTI ULCEROGENIC EFFECT OF ROXATIDINE AND RABEPRAZOLE USING A RAT MODEL

The relationship between nonsteroidal anti-inflammatory drugs (NSAIDs) and gastroduodenal injury is well established. [1] Many factors such as gastric acid, pepsin secretion, gastric microcirculation, prostaglandin E2 (PGE2) content, pro-inflammatory cytokines interleukin(IL)-1 and tumor necrosis factor-α (TNF- α) , contribute to the formation of gastric mucosal damage and subsequently to ulcer development [2-4] . Among the NSAIDs, Aspirin and diclofenac are commonly associated with peptic ulcer disease. [5] Multiple agents, including antacids, H2-receptor antagonists, and proton pump inhibitors, are currently available for the treatment of gastric ulcers. [6] Proton pump inhibitors are the most potent inhibitors of gastric acid secretion. [7] H2-receptor antagonists are other alternative to Proton pump inhibitors and in some studies the H2 receptor antagonists have demonstrated comparable efficacy to them. [8, 9] Roxatidine is the Second Generation H2-Receptor antagonist has longer duration of action with greater 24 hour acid suppression 10 . Rabeprazole is commonly used Proton Pump Inhibitor. Although, both the drugs have been frequently used in various types of peptic ulcer diseases for quite some time, a head to head comparison is still wanting. Therefore, we went ahead to take up this issue to compare the anti- gastric acid secretory and anti-ulcerogenic effect of roxatidine and rabeprazole by using aspirin induced gastric ulcer model of rat. This study can also serve as a platform for the future clinical studies.
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Anti-Ulcerogenic Effect of 2-(Pyrimidinylsulfinyl) Benzimidazole Derivative Against Different Ulcerogenic Agents In Rats

Anti-Ulcerogenic Effect of 2-(Pyrimidinylsulfinyl) Benzimidazole Derivative Against Different Ulcerogenic Agents In Rats

1221 ulcer effect to a particular drug. Ethanol-induced gastric lesion formation may be due to stress in gastric blood flow that contributes to the development of the hemorrhage and necrotic aspects of tissue injury [15].HCl further deepens the necrosis and increase tissue injury. It was observed in this study that the BD reduced significantly ethanol/HCl- induced ulcer. The significant inhibitory effect of BD in ASA and indomethacin-induced ulceration further support the antiulcer effect of 2-(pyrimidinylsulfinyl) benzimidazole derivative. The ulceration induced by ASA is attributed mainly due to the biosynthesis of cytoprotective prostaglandin resulting in overproduction of leukotriene and other products of 5-lipoxygenase pathway [16]. These agents break the mucosal barrier, provoke an increase in gastric mucosal permeability to H + and Na + ions, and drop in the transmucosal potential difference and induce the formation of erosions and ulcers [17]. These results indicate a possible local increase in synthesis of cytoprotective prostaglandin, inhibition of leukotriene and gastric mucosal permeability to H + and Na + ions by BD. Indomethacin, a known ulcerogen especially in an empty stomach [18] causes ulcer mostly on the glandular (mucosal) part of the stomach [19,20].The BD was observed to significantly reduce mucosal damage in the indomethacin– induced ulcer model, suggesting the possible effect of BD and involvement of prostaglandin in the anti ulcer effect of BD.
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NTI ULCEROGENIC EFFECT OF GENISTEIN AGAINST INDOMETHACIN INDUCED GASTRIC ULCER IN RATS

NTI ULCEROGENIC EFFECT OF GENISTEIN AGAINST INDOMETHACIN INDUCED GASTRIC ULCER IN RATS

Our results showed that IND produced gastric ulcer in rats as indicated from gastric ulcer index. According to Sabiu et al. [22], the abnormal elevation of gastric juice acidity by IND may also participate in the augmentation of the severity of gastric ulcer. Choi et al. [23] reported that inflammatory mediators, such as TNF-α, are involved in the pathogenesis of IND-induced gastric ulcer and is one of the aggressive factors in ulcerogenesis. It was documented that TNF-α level is elevated in gastric tissues of IND-treated rats [23], and this came online with our findings. Furthermore, it was proved that there is a relation between TNF-α and PGE2. It was found that exogenous administration of PGE2 produced an anti-ulcer effect by preventing the IND-induced TNF-α increase [24].
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Anti-Ulcerogenic Effect of Some Indian Medicinal Plants on Mucosal Lesion in Rats

Anti-Ulcerogenic Effect of Some Indian Medicinal Plants on Mucosal Lesion in Rats

The phyto-constituents like flavonoids, tannins, terpenoids, and Saponin have been reported in several anti-ulcer literatures as possible gastro protective agents. Flavonoids, tannins and triterpenes are among the cytoprotective active materials for which anti ulcerogenic efficacy has been extensively confirmed (7). Tannins may prevent ulcer development due to their protein precipitating and vasoconstriction effects. Their astringent action can help precipitating micro proteins on the ulcer site, thereby forming an impervious layer over the lining that hinders gut secretions and protects the underlying mucosa from toxins and other irritants (6,34).
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Study on phytochemical profile and anti-ulcerogenic effect of Cayratia pedatata Lam in albino wistar rats

Study on phytochemical profile and anti-ulcerogenic effect of Cayratia pedatata Lam in albino wistar rats

It is well known that pylorus ligation causes gastric hypersecretion due to poorly understood mechanisms. The activation of the vagus-vagal reflex by stimulation of pressure receptors in the antral gastric mucosa in pylorus ligature model is believed to increase gastric tonus and secretion [19] . Digestive effect of the accumulated gastric juice is belived to be responsible for producing ulcers in the pylorus ligated rats. Pylorus ligated induced ulcers are thought to be caused due to increased presence of acid and pepsin in the stomach. The essential criteria, which determine the status of mucosal defense barrier against the offensive assault of acid-pepsin is the quality and quantity of gastric mucus secretion. Increased mucus secretion by the gastric mucosal cells can prevent gastric ulceration by several mechanisms including lessening stomach wall friction during peristalsis and acting as an effective barrier to the back diffusion of hydrogen ions [20] .
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Study on phytochemical profile and Anti-ulcerogenic effect of Casuarina equisetifolia (L.)

Study on phytochemical profile and Anti-ulcerogenic effect of Casuarina equisetifolia (L.)

Their anti-ulcerogenic potency was tested against indomethacin-induced ulcer. Indomethacin is a cyclooxygenase inhibitor which suppresses gastroduodenal bicarbonate secretion, reduces endogeneous prostaglandin biosynthesis and disrupts the mucosal barrier as well as mucosal blood flow in animals [23]. It is also well known that prostaglandins synthetized in large quantities by the gastrointestinal mucosa can prevent experimentally induced ulcers by ulcerogens. Thus, when the ulcers lesions are induced by indomethacin, the cytoprotective effect of the
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Opioid Analgesics Potentiate the Anti-Inflammatory and Inhibit Ulcerogenic Activity of Aspirin.

Opioid Analgesics Potentiate the Anti-Inflammatory and Inhibit Ulcerogenic Activity of Aspirin.

The common recommendation of opioids to treat non inflammatory pains may not be rational in view of reported literature regarding anti inflammatory activity of morphine. In the present study morphine (a mixed agonist), pethidine (predominantly µ agonist) and pentazocine (powerful k agonist) have been investigated for their possible anti-inflammatory and ulcerogenic activity in normal as well as in aspirin treated albino rats for any interactions. Aspirin in the dose of 200 mg/kg and 54 mg/kg p.o., Morphine in the dose of 4.5 mg/kg and 1.5 mg/kg i.m., Pethidine in the dose of 45 mg/kg and 15 mg/kg i.m., Pentazocine in the dose of 13.5 mg/kg and 4.5 mg/kg i.m., were administered in different groups of albino rats to study their effect on inflammation induced by carrageenan or a foreign body. Gastric mucosal studies were also carried out. Therapeutic equivalent doses of these opioids produced significant anti inflammatory activity, almost comparable to that of Aspirin (200 mg/kg).The sub anti-inflammatory dose of opioids potentiated the anti-inflammatory activity of aspirin. The similar dose of these opioids when combined with 200mg/kg and 54 mg/kg of aspirin produced significant gastric ulceration as compared to control, but reduced significantly the ulcerogenic effect of aspirin. Keeping in mind the dependence potential of these opioids, further clinical trials are necessary to establish the efficacy of such combination in the treatment of inflammation.
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ANTI ULCEROGENIC EFFECTS OF ARECA CATECHU L  IN SPRAGUE DAWLEY RATS

ANTI ULCEROGENIC EFFECTS OF ARECA CATECHU L IN SPRAGUE DAWLEY RATS

The aim of this study was to evaluate the anti-ulcerogenic activity of aqueous extract of Areca catechu L in ethanol induced ulcer model in Sprague Dawley Rats. For possible mechanism of anti-ulcerogenic potential, determination of ulcer index was done using the Merazzi-Uberti and Turba method. Also, analytical method was used to test the 10% homogenate preparation of mucosa of the glandular stomach for protein content and glutathione level. The Sprague Dawley Rats were divided into five groups. Group I was the Normal Untreated group. Group II was the alcohol treated group. Group III was the alcohol treated group and protected group using Areca nut extract 1 g/kg.bwt. Group IV was the alcohol treated group and protected using Areca nut extract 2g/kg.bwt. Group V was the alcohol treated group and protected using the positive control Ranitidine 50 mg/kg.bwt .The paper details the rationale of using Areca nut extract to protect the animals from ulcer formation. In conclusion, aqueous extract of areca nut showed potential anti- ulcerogenic effect compared to Ranitidine, which is the standard gastric anti-secretory drug.
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Synthesis and anti-inflammatory activity of some new thiadiazole linked pyrazole benzene sulphonamides as cyclooxygenase inhibitors

Synthesis and anti-inflammatory activity of some new thiadiazole linked pyrazole benzene sulphonamides as cyclooxygenase inhibitors

A new series of thiadiazole linked pyrazole benzenesulfonamide derivatives were synthesized by the condensation of aldehydic pyrazole with aryl substituted thiadiazole amine followed by Schiff base reaction. The synthesized compounds (6a-o) were characterized by IR, NMR, and Mass spectral data, further evaluated their in-vivo anti-inflammatory, analgesic and in- vitro COX-II inhibition assay. The compounds 6b and 6m showed most significant in-vivo anti- inflammatory with 72.33 &71.17% inhibition along analgesic activity having 67.89% and 71.37 % respectively. Their selectivity against COX-II enzyme with selectivity index 67.81 and 66.38 was established for 6b and 6m, which is compared with Celecoxib. During the gastric ulceration study, selected compounds couldn’t observed any ulcerogenic effect on gastric mucosa.The in-silico pharmacokinetic profile and molecular docking study exposed very good binding affinity towards the Cyclooxygenase (COX-II) enzyme (PDB Id: 3PGH), therefore the compounds 6b and 6m are used as promising lead candidates for the support of drug development.
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EFFECT OF CERTAIN POLYMERS ON THE ULCEROGENIC ACTIVITY OF A NON STEROIDAL ANTI INFLAMMATORY DRUG

EFFECT OF CERTAIN POLYMERS ON THE ULCEROGENIC ACTIVITY OF A NON STEROIDAL ANTI INFLAMMATORY DRUG

techniques of choice in order to coat the drug so as to improve bioavailability and stability and also target a drug at specific sites. The ratio of (1:3) drug to polymer from all polymers used from solid dispersions systems and the best ratio from microbeads were selected to conduct further in vivo evaluation, since it was the best ratio which achieved significant reduction in the release of diclofenac at acidic pH of the stomach and maximal release at alkaline pH of the intestine. The obtained In vivo results indicate that microencapsulation technique was able to protect the stomach from ulcerogenic effect of diclofenac compared to solid dispersion technique.
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Journal of Applied Pharmaceutical Science

Journal of Applied Pharmaceutical Science

activity of CLL as observed. The antioxidant activity of putative antioxidants have been attributed to various mechanisms, among which are prevention of chain initiation, binding of transition metal ion catalysts, decomposition of peroxides, prevention of continued hydrogen abstraction, reductive capacity and radical scavenging (Oktay et al., 2003). The HPLC profiling of the extract and fraction reveal preconcentration of the polyphenols in EAF than the aqueous crude extract. Trans-cinnamic acids glucosides constitute 21.9% of these polyphenols in EAF. Present evaluation of the polar fractions and crude extract revealed the concentration of TPC to be 61.33, 78.67, 90.78 and 136.22 µg/ml for ETF, EAF, CEAE and CETE, respectively. The crude extract is richer in polyphenolic than the fraction. This result may in part be due to the presence in the crude extract many different phenolics components that were not isolated by EAF during the fractionation process. Different mechanisms have been proposed for the pathogenesis of cysteamin-induced gastrointestinal ulcer such as hypersecretion of gastric acid, reduced bicarbonate secretion in response to acid in duodenum and delayed gastric emptying (Szabo, 1987; Szabo, 1978; Poulsen et al., 1985).The results obtained shows that CLL EAF inhibited the formation of duodenal ulcer. This effect might be due to gastric acid inhibition or neutralization in the stomach or due to stimulation of the formation of mechanical adherent barrier (mucus) by EAF in the duodenum. Other possible mechanisms reported in literature are by stimulation of epidermal growth factor (EGF), endothelium-derived relaxing factor (nitric oxide) and non- protein sulfydryl derivatives, all are involved in maintaining the integrity of the mucosa (Salim, 1989; Donadel et al.,2005). It is also
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MUCOADHESIVE MICROCAPSULES OF INDOMETHACIN: EVALUATION FOR CONTROLLED RELEASE AND ULCEROGENIC ACTIVITY

MUCOADHESIVE MICROCAPSULES OF INDOMETHACIN: EVALUATION FOR CONTROLLED RELEASE AND ULCEROGENIC ACTIVITY

Mucoadhesive microcapsules of indomethacin were prepared by an emulsification-ionic gelation process employing sodium carboxy methylcellulose, methylcellulose, Carbopol and hydroxy propyl methyl cellulose along with alginate and the microcapsules were evaluated for release kinetics and ulcerogenic activity. The resulting microcapsules were discrete, free flowing, multinucleate, monolithic and spherical. Microencapsulation efficiency was 41-70 % and relatively high with alginate-sodium carboxymethylcellulose. Indomethacin release from these mucoadhesive microcapsules was found to be slow and extended over longer periods of time and depended on the composition of coat and size of the microcapsules. Drug release was diffusion controlled and followed first order kinetics. Alginate-methyl cellulose and alginate-sodium carboxymethylcellulose microcapsules were found suitable for oral controlled release. The microcapsules exhibited good mucoadhesive property in the in vitro wash-off test. Release from some microcapsules fulfilled the official (USP 23) drug release test-2 requirement of indomethacin extended release capsules. A 62-80 % reduction in ulcerogenic activity was observed with these microcapsules when compared to pure drug indomethacin.
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 A COMPREHENSIVE REVIEW ON THETRAN VIDHAI KUDINEER: A SIDDHA POLYHERBAL FORMULATION

 A COMPREHENSIVE REVIEW ON THETRAN VIDHAI KUDINEER: A SIDDHA POLYHERBAL FORMULATION

Terminalia chebula is a moderate tree used in traditional medicines. It is belongs to the family combretaceae and commonly called as Black myrobalan, Ink tree (or) Chebulic myrobalan and also known as “King of medicine” due to its wide spectrum of pharmacological activities associated with the biologically active chemicals present in this plant. It is used for the treatment of number of diseases like cancer, paralysis, cardio vascular diseases, ulcers, leprosy, arthritis, gout, epilepsy etc. It has beneficial effect on all the tissues 6 . (Table 5,6)
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THE ANTI ULCEROGENIC ACTIVITY OF THE CRUDE METHANOLIC EXTRACT OF MONECHMA CILIATUM SEEDS

THE ANTI ULCEROGENIC ACTIVITY OF THE CRUDE METHANOLIC EXTRACT OF MONECHMA CILIATUM SEEDS

This study was carried out to evaluate the anti-ulcerogenic activity of the methanolic extract of Monechma ciliatum seeds to validate its traditional uses in treatment of stomach disturbances. The methanolic extract of Monechma ciliatum seeds was screened for its anti- ulcerogenic activity against induced-ulcer in four different models. The phytochemical screening of the plant showed that flavonoids, sterols, alkaloids, triterpenes, tannins and saponins are the main constituents of the plant. The results showed that the methanolic extract of Monechma ciliatum seeds at a dose 300mg/kg markedly decreased the incidence of ulcer induced by oral administration of ethanolic HCl in mice by 81.86% ulcer inhibition where as sucralfate showed 50.54% ulcer inhibition, as well as it significantly inhibited ulcer induced by water immersion stress in rats by 86.92%ulcer inhibition, whereas omeprazole showed 100% ulcer inhibition. Also the extract reduced ulcer index compared with the control (10.66±0.53 – 14.72±0.65) in aspirin-induced ulcer. At a dose 400µg/ml the extract elevated stomach pH{H + } to (0.0015) compared with pH {H + } (0.0050) induced by histamine( 2 µg/ml). The results obtained from this study revealed that the methanolic extract of M.ciliatum seeds possesses anti-ulcerogenic activity.
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Anti-Ulcerogenic Effects of Salmalia Malabarica in Gastric Ulceration – Pilot Study

Anti-Ulcerogenic Effects of Salmalia Malabarica in Gastric Ulceration – Pilot Study

of acid in GIT  [20]. Hence NSAIDs correspond to the initial stages of destruction of the muco- sal cell membrane, parietal cells and endothelial cells [42]. Prostaglandins play a crucial role in the maintenance of gastroduodenal mucosal integrity and repairing of GIT [43]. NSAIDs also cause dis- turbance in prostaglandin synthesis and thus can damage mucosal defense. Arachidonic acid orig- inates from membrane phospholipids by the en- zyme phospholipase A2. The metabolism of ara- chidonic acid to prostaglandins is catalyzed by the cyclooxygenase (COX) pathway [44]. COX-1 and COX-2 are 2  isoforms having similarity in their amino acid sequences but have different roles in the pathophysiological cascade of events [45]. As- pirin is a potent COX blocker which also decreases gastroduodenal bicarbonate secretion [46]. Ulcers induced by NSAIDs resulted in the production of excess amounts of acid leading to pyloric obstruc- tion and mucosal necrosis. Although various fac- tors are involved for the induction of ulcerogen- esis, the most important is an imbalance between offensive and defensive factors. Methanol extract of Salmalia malabarica significantly decreased the ulcer index in aspirin-induced ulcer and in- creased the percentage of protection up to 74.54%, as shown in Fig. 1 and Table 1. Methanol extract of Salmalia malabarica showed its anti-ulcerogenic
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ANTI  INFLAMMATORY, ANALGESIC & ULCEROGENIC ACTIVITY OF KETOPROFEN GLUCOPYRANOSIDE CONJUGATES

ANTI INFLAMMATORY, ANALGESIC & ULCEROGENIC ACTIVITY OF KETOPROFEN GLUCOPYRANOSIDE CONJUGATES

It is a well accepted fact that gastrointestinal lesions produced by NSAIDs are due to two different mechanisms: (a) direct contact with gastric mucosa through oral dose and (b) systemic effect which may be manifested by after intravenous dosing 6 . Masking the acidic group of NSAIDs with a view to decrease the gastrointestinal toxicity due to direct injury has been postulated 7- 10 . The purpose of this study was to mask the free acidic group by synthesizing its glucopyranoside derivative and evaluate its anti-inflammatory activity, analgesic activity and gastrointestinal toxicity.
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BIOCHEMICAL STUDIES ON THE ANTI ULCEROGENIC POTENTIAL OF CARDIOSPERMUM HALICACABUM L  SEEDS

BIOCHEMICAL STUDIES ON THE ANTI ULCEROGENIC POTENTIAL OF CARDIOSPERMUM HALICACABUM L SEEDS

DISCUSSION: Seed oils of C. halicacabum varieties significantly reduced the formation of gastric ulcer in ethanol induced ulcer rat model. A dose dependent response on the intensity of gastric ulceration was noted. However, statistically more effect was noted in var. microcarpum. The increase in potassium content is significant because it alters the hydrogen ion content there by increasing the mucosal protective action. The mucosal defense mechanism may be due to the epithelial cells of the gastric mucosa which are impermeable to hydrogen ions thereby forming a physical barrier 26 . Carbohydrate and protein ratio also supports the above observation. Difference between the two seed oils may be due to the quantitative variation of the biological compounds.
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Anti Ulcerogenic Activity of the Pomegranate Peel (Punica granatum) Methanol Extract

Anti Ulcerogenic Activity of the Pomegranate Peel (Punica granatum) Methanol Extract

There are no related reports which describe antiulcer effect of pomegranate peel but in other studies fruit parts are assessed. Although the exact mechanism of the anti-ulcer activities of pomegranate peel has not been clearly delineated, it contains some active constituents which ulcer protective properties have been identified based on their antioxidant activity. Pomegranate is a rich source of polyphenols. It contains antioxidants like solu- ble polyphenols, tannins, and anthocyanins which pos- sessing anti-atherosclerotic properties. The in vitro eva- luation of the pomegranate extracts and some selected medicinal plants on H pylori activity demonstrate that the extract of pomegranate has remarkable anti-H. pylori function [24].
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