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芝麻酚通过其不依赖环氧化酶的抗氧化作用减轻双氯芬酸诱导的大鼠急性胃黏膜损伤。

Sesamol attenuates diclofenac-induced acute gastric mucosal injury via its cyclooxygenase-independent antioxidative effect in rats.

作者信息

Hsu Dur-Zong, Chu Pei-Yi, Li Ya-Hui, Liu Ming-Yie

机构信息

Department of Environmental and Occupational Health, National Cheng Kung University Medical College, National Cheng Kung University, Tainan, Taiwan.

出版信息

Shock. 2008 Oct;30(4):456-62. doi: 10.1097/SHK.0b013e3181672185.

DOI:10.1097/SHK.0b013e3181672185
PMID:18277948
Abstract

We examined the protective effects of sesamol against acute gastric mucosal damage induced in rats by nonsteroidal anti-inflammatory drug diclofenac (DLF). We also measured the ulcer index, nitrite, iNOS, lipid peroxidation, hydroxyl radical, superoxide anion, reduced glutathione levels, prostaglandin E2, mucus, and cyclooxygenase activity in the rat mucosa. Sesamol attenuated gastric ulcer, nitrite, and iNOS in DLF-treated stomachs. Sesamol reduced mucosal lipid peroxidation and hydroxyl radical levels; however, neither DLF nor sesamol affected mucosal superoxide anion production. In addition, sesamol significantly maintained the reduced mucosal glutathione levels in DLF-treated stomachs of rats. Sesamol did not affect mucosal mucus production, but it further decreased DLF-induced mucosal prostaglandin E2 generation and cyclooxygenase activity. Therefore, sesamol might protect gastric mucosa against DLF-induced injury by inhibiting hydroxyl radical-associated lipid peroxidation. In addition, the cyclooxygenase pathway may not be involved in sesamol's gastric mucosal protection.

摘要

我们研究了芝麻酚对非甾体抗炎药双氯芬酸(DLF)诱导的大鼠急性胃黏膜损伤的保护作用。我们还测量了大鼠胃黏膜中的溃疡指数、亚硝酸盐、诱导型一氧化氮合酶(iNOS)、脂质过氧化、羟自由基、超氧阴离子、还原型谷胱甘肽水平、前列腺素E2、黏液和环氧化酶活性。芝麻酚减轻了DLF处理的胃中的胃溃疡、亚硝酸盐和iNOS水平。芝麻酚降低了黏膜脂质过氧化和羟自由基水平;然而,DLF和芝麻酚均未影响黏膜超氧阴离子的产生。此外,芝麻酚显著维持了DLF处理的大鼠胃中黏膜还原型谷胱甘肽水平。芝麻酚不影响黏膜黏液的产生,但它进一步降低了DLF诱导的黏膜前列腺素E2生成和环氧化酶活性。因此,芝麻酚可能通过抑制与羟自由基相关的脂质过氧化来保护胃黏膜免受DLF诱导的损伤。此外,环氧化酶途径可能不参与芝麻酚对胃黏膜的保护作用。

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