Morphologic and pharmacological investigations in the epicatechin gastroprotective effect.

A L Rozza,A Tanimoto,C A Hiruma-Lima,C H Pellizzon

doi:10.1155/2012/708156

A L Rozza, A Tanimoto + Show 2 more

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https://doi.org/10.1155/2012/708156

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Abstract

Previous studies of the gastroprotective activity of plants have highlighted the importance of the polyphenolic compound epicatechin (EC) in the treatment of gastric ulcers. This paper aimed to evaluate and characterize the gastroprotective mechanism of action of EC using male rats. The gastroprotective action of EC was analyzed in gastric ulcers induced by ethanol or indomethacin. The involvement of sulfhydryl (SH) groups, K+ ATP channels, α 2 adrenoceptors, gastric antisecretory activity, and the amount of mucus in the development of gastric ulcers were investigated. The lowest effective dose of EC providing gastroprotective effects was 50 mg/kg in the ethanol-induced gastric ulcers and 25 mg/kg in the indomethacin-induced gastric ulcers. The gastroprotection seen upon treatment with EC was significantly decreased in rats pretreated with a SH compound reagent or an α 2-receptor antagonist, but not with a K+ ATP channel blocker. Furthermore, oral treatment with EC increased mucus production and decreased H+ secretion. Immunohistochemistry demonstrated the involvement of superoxide dismutase (SOD), nitric oxide (NO), and heat shock protein-70 (HSP-70) in the gastroprotection. These results demonstrate that EC provides gastroprotection through reinforcement of the mucus barrier and neutralization of gastric juice and this protection occurs through the involvement of SH compounds, α 2-adrenoceptors, NO, SOD, and HSP-70.

Highlights

Gastric ulcers affect thousands of people worldwide and are considered a global health problem
According to Tukey’s test, there was no significant difference between the ulcer areas of the groups treated with 50 mg/kg or 75 mg/kg; the dose of 50 mg/kg was used for all subsequent experiments
Motawi et al [20] previously demonstrated that an elevation in gastric acid secretion, neutrophil infiltration, and alterations in nitric oxide (NO) production and oxidative stress are mechanisms that contribute to indomethacin-induced ulceration

Summary

Introduction

Gastric ulcers affect thousands of people worldwide and are considered a global health problem. Agents that may initiate the development of an ulcer include the following: acid and pepsin secretion, Helicobacter pylori infection, poor diet, alcohol ingestion, and the use of nonsteroidal antiinflammatory drugs (NSAIDs). Protective factors include the following: an intact mucosal barrier, adequate mucus secretion and blood flow, cellular regeneration, prostaglandin secretion, and epidermal growth factor release [1, 2]. The current treatment options for patients suffering from gastric ulcers include antacids, sucralfate, prostaglandins, muscarinic antagonists, histamine-2 receptor antagonists, and proton pump inhibitors. The long-term use of these drugs may cause side effects such as hypersensitivity, arrhythmia, impotence, gynecomastia, and hematopoietic disturbances [3]. Their use does not necessarily prevent the recurrence of the disease

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