氧自由基和细胞凋亡在大鼠应激性溃疡中的作用

目的探讨氧化应激与细胞凋亡在应激性溃疡发病中的作用及相关性。方法改良Allen法制造颅脑损伤并发应激性溃疡模型，40只大鼠随机分为正常对照组和应激后3、6、12、24小时组。测定溃疡指数（UI）、胃黏膜超氧化物歧化酶（SOD）和丙二醛（MDA）；透射电镜及流式细胞仪检测早期细胞凋亡。结果颅脑损伤6小时后各应激组UI增加（P〈0．05）；胃黏膜SOD下降，MDA升高（P〈0．05），与对照组相比应激后3小时差异即有显著性，6—12小时达高峰（P〈0．05）；早期细胞凋亡率于应激后6小时开始显著增多，12小时达高峰（P〈0．05）；应激后6小时透射电镜可见凋亡细胞，12小时显著增多达高峰。应激后MDA与早期细胞凋亡率呈显著正相关（r=0．684，P〈0．05），SOD活性与早期细胞凋亡率呈显著负相关（r=-0．713，P〈0．05）。结论细胞凋亡参与急性胃黏膜损伤；氧化应激是应激性胃黏膜损害的重要因素，可能参与细胞凋亡。

Effect of Oxygen Free Radical and Apoptosis on Stress Ulcer in Rats

Objective To investigate the effects of oxidative stress and apoptosis on the pathogenesis of stress ulcer and the correlation between them. Methods The rat model of acute craniocerebral injury complicated with stress ulcer was duplicated by modified Allen＇s method. Forty rats were randomly divided into control group and four model groups （3,6, 12, and 24 hours after stress）. The ulcer indexes （UI） and the contents of malondi- aldehyde （MDA） and superoxide dismutase （SOD） of mucosa tissues were detected. The index of earlier ap- optosis was detected by both flow cytometry （FCM） and transmission electron microscopy （TEM）. Results The UI grew with time 6 hours after stress （ P 〈 0.05 ）. The activities of SOD decreased while the levels of MDA increased after stress. The significant change was detected 3 hours later and increased to a peak at 6-12 hours （P 〈 0. 05 ）. Change of the indexes of earlier apoptosis by FCM remarkably increased at 6 hours and reached the peak at 12 hours （ P 〈 0. 05 ）. The apoptotic cell number reached the peak at 12 hours. The ratio of apoptosis was was detected at 6 hours under TEM, and the significantly correlated with the values of MDA （r = 0. 684, P 〈 0.05 ） and negatively correlated with SOD in stress groups （ r = - 0. 713, P 〈 0.05 ）. Conclusions Apoptosis may be involved in the process of acute gastric mucosa injury. As an important impaired factor, oxidative stress may lead to the formation of apoptosis.