#gastroprotective

EVALUATION OF THE GASTROPROTECTIVE AND SUB-CHRONIC TOXICITY OF METHANOL STEM BARK EXTRACT OF XIMENIA AMERICANA LINN (OLACACEAE) IN MALE WISTAR RATS

EVALUATION OF THE GASTROPROTECTIVE AND SUB-CHRONIC TOXICITY OF METHANOL STEM BARK EXTRACT OF XIMENIA AMERICANA LINN (OLACACEAE) IN MALE WISTAR RATS

Abstract:

Ximenia americana is a plant used traditionally in northern parts of Nigeria for treatment of leprotic ulcers and mouth ulcers in addition to other medicinal uses. It contains flavanoids, saponins, tannins among others that has been reported…

Numerous studies have shown that use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with various gastric mucosal lesions, L-carnitine, protects the biological membranes against lipid peroxidation. It has recently been shown that L-carnitine has a gastroprotective effect on gastric mucosa. RESULTS: The intragastric administration of indomethacin induced hyperemia and hemorrhagic erosions in the rat stomachs. L-carnitine significantly prevented gastric ulcerogenesis induced by indomethacin and decreased the ulcer index macroscopically and histopathologically. CONCLUSION: L-carnitine decreases indomethacin-induced gastric mucosal injury and this gastroprotective effect may be attributed to its well-known antioxidant effect.

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Folia Med (Plovdiv). 2006;48(3-4):86-9.

Gastroprotective effect of L-carnitine on indomethacin-induced gastric mucosal injury in rats: a preliminary study.

Erkin B, Dokmeci D, Altaner S, Turan FN.

Source

Department of Pharmacology, Faculty of Medicine, Trakya University Edirne, Turkey.

Abstract

BACKGROUND:

Numerous studies have shown that use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with various gastric mucosal lesions, collectively referred to as NSAID gastropathy, but the detailed mechanism is still not properly understood. L-carnitine, a vitamin-like substance, is a naturally occurring enzymatic antioxidant with a potent free oxygen radical quencher and scavenger capacity; it protects the biological membranes against lipid peroxidation. It has recently been shown that L-carnitine has a gastroprotective effect on gastric mucosa. To our knowledge, the role of L-carnitine on NSAIDs-induced gastric mucosal injury is undefined.

AIM:

The aim of the present study was to determine the gastroprotective effect of L-carnitine on indomethacin-induced gastric mucosal lesions in the rat stomachs.

MATERIAL AND METHODS:

In our study, gastric mucosal injury was induced by the intragastric administration of indomethacin (30 mg/kg). L-carnitine (10, 50, 100 mg/kg) was given to rats by gavage 30 min before the indomethacin administration. The animals were killed 3 h after administration of indomethacin. The stomach of each animal was removed. Mucosal damage was evaluated with macroscopic study and histopathologically.

RESULTS:

The intragastric administration of indomethacin induced hyperemia and hemorrhagic erosions in the rat stomachs. L-carnitine significantly prevented gastric ulcerogenesis induced by indomethacin and decreased the ulcer index macroscopically and histopathologically.

CONCLUSION:

L-carnitine decreases indomethacin-induced gastric mucosal injury and this gastroprotective effect may be attributed to its well-known antioxidant effect.

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Statin Drug Protects Against Ulcers Gastroprotective effect of simvastatin against indomethacin-induced gastric ulcer Simvastatin significantly increased the gastric mucosal total nitrite and prostaglandin E(2) levels. Additionally, simvastatin attenuated the elevations in gastric mucosal superoxide dismutase observed with indomethacin. The gastroprotective effect afforded by simvastatin was significantly augmented by coadministration with L-arginine (a nitric oxide precursor) and inhibited by coadministration with L-NAME (a nitric oxide synthase inhibitor). Results confirm a gastroprotective effect for simvastatin

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Eur J Pharmacol. 2009 Apr 1;607(1-3):188-93. Epub 2009 Feb 13.

Gastroprotective effect of simvastatin against indomethacin-induced gastric ulcer in rats: role of nitric oxide and prostaglandins.

Heeba GH, Hassan MK, Amin RS.

Source

Department of Pharmacology and Toxicology, Faculty of Pharmacy, Minia University, 6111, Egypt. [email protected]

Abstract

This study investigated the possible mechanisms underlying the gastroprotective effect of simvastatin against indomethacin-induced gastric ulcer in rats. Rats were randomly assigned to vehicle-, simvastatin-, simvastatin+L-arginine- and simvastatin+N(G)-nitro-L-arginine methyl ester (L-NAME)-pretreated groups for two weeks. Pyloric ligation was performed for the collection of gastric juice, and gastric ulceration was induced by a single intraperitoneal injection of indomethacin (30 mg/kg). Gastric juice parameters (total acid output, pepsin activity and mucin concentration) were determined. The stomachs tissues were used for determination of gastric mucosal lipid peroxides, superoxide dismutase, catalase, total nitrites and prostaglandin E(2) levels. Pretreatment with simvastatin (10 mg/kg, orally, for 2 weeks) caused significant reduction in gastric mucosal lesions and lipid peroxides associated with a significant increase in gastric juice mucin concentration. Simvastatin significantly increased the gastric mucosal total nitrite and prostaglandin E(2) levels. Additionally, simvastatin attenuated the elevations in gastric mucosal superoxide dismutase observed with indomethacin. The gastroprotective effect afforded by simvastatin was significantly augmented by coadministration with L-arginine (a nitric oxide precursor) and inhibited by coadministration with L-NAME (a nitric oxide synthase inhibitor). Results confirm a gastroprotective effect for simvastatin, and indicate that the anti-ulcer effect of simvastatin is mediated by scavenging free radicals, increasing nitric oxide and prostaglandin E(2) levels, and increasing gastric juice mucin production. We conclude that simvastatin represents a more suitable antihyperlipidemic therapy for patients who are at risk of gastric ulcers that were induced by the use of nonsteroidal anti-inflammatory drugs (NSAIDs).

Read more at www.ncbi.nlm.nih.gov