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前列腺素E2对胃刺激性诱导的细胞凋亡的影响。

Effects of prostaglandin E2 on gastric irritant-induced apoptosis.

作者信息

Hoshino Tatsuya, Takano Tatsunori, Tsutsumi Shinji, Tomisato Wataru, Tsuchiya Tomofusa, Mizushima Tohru

机构信息

Faculty of Pharmaceutical Sciences, Okayama University, Japan.

出版信息

Dig Dis Sci. 2002 Oct;47(10):2370-9. doi: 10.1023/a:1020164000898.

Abstract

We previously reported that various gastric irritants induced both apoptosis and necrosis in cultured gastric mucosal cells. In a continuation of this work, the present study has examined the effects of prostaglandin E2 (PGE2), a cytoprotective factor for gastric mucosa in vivo, on gastric irritant-induced apoptosis and necrosis in vitro. PGE2 inhibited ethanol-induced apoptosis and increased cell viability in a dose-dependent manner in primary cultures of guinea pig gastric mucosal cells. PGE2 also inhibited hydrogen peroxide-induced apoptosis. In contrast, PGE2 showed no cytoprotective effects against ethanol-induced necrosis. Based on these results, we consider that the cytoprotective effects of PGE2 on gastric mucosa in vivo can be partially explained by its inhibitory effect on gastric irritant-induced apoptosis.

摘要

我们之前报道过,多种胃刺激物可诱导培养的胃黏膜细胞发生凋亡和坏死。在这项工作的延续研究中,本研究检测了前列腺素E2(PGE2)(一种体内胃黏膜的细胞保护因子)对体外胃刺激物诱导的凋亡和坏死的影响。在豚鼠胃黏膜细胞原代培养中,PGE2以剂量依赖的方式抑制乙醇诱导的凋亡并提高细胞活力。PGE2还抑制过氧化氢诱导的凋亡。相比之下,PGE2对乙醇诱导的坏死没有细胞保护作用。基于这些结果,我们认为PGE2在体内对胃黏膜的细胞保护作用可部分归因于其对胃刺激物诱导的凋亡的抑制作用。

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