巯基参与胃粘膜防御机制

INVOLVEMENT OF SULFHYDRYLS IN THE PROTECTIVE MECHANISM OF GASTRIC MUCOSA

本工作研究了胃粘膜非蛋白质巯基物质(NPSH)在粘膜防御功能中的作用。结果表明,酸性乙醇灌胃或冷冻加束缚应激引起大鼠胃粘膜 NPSH 含量显著下降;补充含-SH 的化合物半胱胺或还原型谷胱甘肽可防止酸性乙醇引起的胃粘膜损伤;在酸性乙醇灌胃或应激后,胃粘膜谷胱甘肽还原酶活性明显降低,并与 NPSH 含量的下降在时间上一致;丙二醛含量在酸性乙醇灌胃后显著升高,自由基清除剂二甲亚砜可减轻胃粘膜损伤。上述结果提示,胃粘膜NPSH 可能通过对自由基的清除作用参与粘膜的局部防御机制;谷胱甘肽还原酶活性下降和自由基生成增加所导致的粘膜 NPSH 含量下降可能是损伤发生过程的重要环节。

The present work have studied the role of nonproteinsulfhydryl(NPSH)in theprotective mechanism of gastric mucosa.During the development of gastric in-jury induced by acidified ethanol(AE)gavage or restraint-cold stress(RCS),NPSHcontent in gastric mucosa markedly decreased.Pretreatment with cysteamine(cys)or reductive glutathione(GSH)could prevent gastric mucosa from injury inducedby AE.The activity of glutathione reductase in gastric mucosa was inhibited con-sistently in the time course with NPSH decrease after AE gavage or RCS.Malon-dialdehyde(MDA)level in the mucosa increased after AE gavage and dimethylsuloxide,a free radical scavenger,could reduce AE induced injury.The aboveresults suggest that NPSH in gastric mucosa might be involved in the local protectivemechanism through its free radical scavenging activity,and the decrease of NPSHin gastric mucosa resulted by the inhibition of glutathione reductase activity andthe increase of free radical production may be an important step in the developmentof injury.