生长抑素对氧自由基引起的离体胃粘膜细胞损伤的保护作用及其机制

采用pronase—EDTA法分离大鼠胃粘膜细胞,将黄嘌呤氧化酶(xanthineoxidase,XO)—黄嘌呤(xanthine,X)氧自由基生成系统加入培养液诱发细胞的损伤。观察到预先加入生长抑素可以剂量依赖性地减轻XO—X引起的细胞死亡和乳酸脱氢酶的漏出;同时抑制XO—X引起的细胞脂质过氧化水平的升高,并翻转细胞膜流动性及溶血性卵磷脂与卵磷脂比值的变化。上述结果提示,生长抑素对氧自由基引起的胃粘膜细胞损伤可能具有直接的保护作用,其机制似与防止质膜的脂质过氧化并从而保护细胞膜免受损伤有关。

PROTECTIVE EFFECT OF SOMATOSTATIN ON THE OXYGEN RADICAL-INDUCED INJURY OF ISOLATED GASTRIC MUCOSAL CELLS AND ITS MECHANISM

In the present work, the rat gastric mucosal cells isolated with the pronase-EDTA method were injured by oxygen radicals produced by xanthine oxidase-xanthine(XO-X). It was observed that addition of somatostatin into the media could reduce the cellular mortality and the leakage of lactate dehydrogenase from the cells, inhibit the increase in the level of cellular lipid peroxides and reverse the changes in the cellular membrane fluidity and the ratio between lysolecithin and lecithin (LPC/ PC) induced by XO-X. These suggested that somatostatin might protect the gastric mucosal cells from oxygen radical-induced injury directly and its mechanism might be related to the protection of the cellular membrane through prevention of lipid peroxidation by oxygen radicals.