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巯基在胃黏膜保护机制中的作用

[Involvement of sulfhydryls in the protective mechanism of gastric mucosa].

作者信息

Li T, Zhang X J

机构信息

Department of Physiology, Beijing Medical University.

出版信息

Sheng Li Xue Bao. 1990 Dec;42(6):571-7.

PMID:2293370
Abstract

The present work have studied the role of nonproteinsulfhydryl (NPSH) in the protective mechanism of gastric mucosa. During the development of gastric injury induced by acidified ethanol (AE) gavage or restraint-cold stress (RCS), NPSH content in gastric mucosa markedly decreased. Pretreatment with cysteamine (cys) or reductive glutathione (GSH) could prevent gastric mucosa from injury induced by AE. The activity of glutathione reductase in gastric mucosa was inhibited consistently in the time course with NPSH decrease after AE gavage or RCS. Malondialdehyde (MDA) level in the mucosa increased after AE gavage and dimethyl suloxide, a free radical scavenger, could reduce AE induced injury. The above results suggest that NPSH in gastric mucosa might be involved in the local protective mechanism through its free radical scavenging activity, and the decrease of NPSH in gastric mucosa resulted by the inhibition of glutathione reductase activity and the increase of free radical production may be an important step in the development of injury.

摘要

本研究探讨了非蛋白巯基(NPSH)在胃黏膜保护机制中的作用。在酸化乙醇(AE)灌胃或束缚-冷应激(RCS)诱导的胃损伤发展过程中,胃黏膜中NPSH含量显著降低。用半胱胺(cys)或还原型谷胱甘肽(GSH)预处理可预防AE诱导的胃黏膜损伤。AE灌胃或RCS后,胃黏膜中谷胱甘肽还原酶的活性随NPSH的降低而持续受到抑制。AE灌胃后,黏膜中丙二醛(MDA)水平升高,自由基清除剂二甲基亚砜可减轻AE诱导的损伤。上述结果表明,胃黏膜中的NPSH可能通过其自由基清除活性参与局部保护机制,而谷胱甘肽还原酶活性的抑制和自由基产生的增加导致胃黏膜中NPSH的减少可能是损伤发展的重要步骤。

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