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表儿茶素胃保护作用的形态和药理学研究。

Morphologic and pharmacological investigations in the epicatechin gastroprotective effect.

机构信息

Morphology Department, Biosciences Institute, UNESP-University Estadual Paulista, P.O. Box 510, 18618-970 Botucatu, SP, Brazil.

出版信息

Evid Based Complement Alternat Med. 2012;2012:708156. doi: 10.1155/2012/708156. Epub 2012 May 14.

DOI:10.1155/2012/708156
PMID:22666296
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3359827/
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.

摘要

先前有关植物胃保护活性的研究强调了多酚化合物表儿茶素(EC)在治疗胃溃疡中的重要性。本文旨在评估和表征 EC 对雄性大鼠的胃保护作用机制。分析了 EC 对乙醇或吲哚美辛诱导的胃溃疡的胃保护作用。研究了巯基(SH)基团、K+(ATP)通道、α2 肾上腺素能受体、胃分泌抑制活性以及发展中胃溃疡的粘蛋白量在胃保护作用中的作用。在乙醇诱导的胃溃疡中,EC 的最低有效剂量为 50mg/kg,在吲哚美辛诱导的胃溃疡中,EC 的最低有效剂量为 25mg/kg。在用 SH 化合物试剂或 α2-受体拮抗剂预处理的大鼠中,EC 治疗的胃保护作用明显降低,但用 K+(ATP)通道阻滞剂预处理则不然。此外,口服给予 EC 可增加粘蛋白的产生并减少 H+分泌。免疫组织化学显示超氧化物歧化酶(SOD)、一氧化氮(NO)和热休克蛋白 70(HSP-70)参与了胃保护作用。这些结果表明,EC 通过增强粘液屏障和中和胃液来提供胃保护作用,这种保护作用通过 SH 化合物、α2-肾上腺素能受体、NO、SOD 和 HSP-70 的参与来实现。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5451/3359827/57238d5cc99e/ECAM2012-708156.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5451/3359827/dff810b806b4/ECAM2012-708156.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5451/3359827/54ee06b04c96/ECAM2012-708156.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5451/3359827/99dac2461fc0/ECAM2012-708156.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5451/3359827/cfba608e39ae/ECAM2012-708156.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5451/3359827/6cf7a95637c4/ECAM2012-708156.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5451/3359827/57238d5cc99e/ECAM2012-708156.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5451/3359827/dff810b806b4/ECAM2012-708156.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5451/3359827/54ee06b04c96/ECAM2012-708156.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5451/3359827/99dac2461fc0/ECAM2012-708156.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5451/3359827/cfba608e39ae/ECAM2012-708156.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5451/3359827/6cf7a95637c4/ECAM2012-708156.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5451/3359827/57238d5cc99e/ECAM2012-708156.006.jpg

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