氧自由基和细胞凋亡在大鼠应激性溃疡中的作用

　　【摘要】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和应激后3、6、12、24h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6h后各应激组UI增加;胃黏膜SOD下降，MDA升高，于应激后3h即有显著变化，6～12h达高峰;早期细胞凋亡率于应激后6h开始显著增多，12h达高峰;应激后6h透射电镜可见凋亡细胞，12h显著增多达高峰。SOD、MDA变化分别与细胞凋亡率的变化呈显著相关性，且时间上早于后者。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，可能参与导致细胞凋亡。

　　关键词:氧自由基;细胞凋亡;应激性溃疡发病机制

　　Effect of oxygen free radical and apoptosis on stress ulcer in rats

　　Wang Tianyi,Zhu Yuqun,Yang Zhaoxu

　　Department of Gastroenterology,Tiantan Hospital Affiliated to Capital University of Medical Science,Beijing 100050.

　　【Abstract】ObjectiveTo investigate the effects of oxidative stress and apoptosis on the pathogenesis of stress ulcer and the correlation between them.MethodsThe rat model of acute craniocerebral injury complicated with stress ulcer was duplicated by modified Allen’s.40 rats were randomly divided into control group and 3,6,12,24h groups after stress.The ulcer indexes(UI)and the contents of SOD and MDA of mucosa tissues were detected.The index of earlier apoptosis was detected by both FCM and transmission electron microscope(TEM).ResultsThe UI grew with time after stress 6h.The activities of SOD decreased while the levels of MDA increased after stress.The significant change was detected at 3h and rose to a peak at 6～12h.Change of indexes of earlier apoptosis by FCM increased obviously at 6h,and the peak was at 12h.The apoptotic cell was detected at 6h under TEM,and the number peaked at 12h.The indexes of oxidative stress had a closed correlation with the ratio of apoptosis,but occurred earlier than the latter.ConclusionApoptosis 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.

　　Key wordsoxygen free radicalapoptosisstress ulcerpathogenesis

　　应激性溃疡(stress ulcer,SU)的发病机制尚未完全阐明。目前认为胃黏膜微循环障碍造成黏膜缺血、缺氧是重要的发病环节。氧化应激是机体遭受应激后的重要反应

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