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机构地区:[1]中山大学附属第二医院消化科,广东广州510120 [2]中山大学附属第五医院
出 处:《胃肠病学和肝病学杂志》2012年第6期550-553,共4页Chinese Journal of Gastroenterology and Hepatology
基 金:广东省自然科学基金(2009B030801142)
摘 要:目的探讨COX-2在氯丙嗪所致大鼠药物性肝损伤中的作用。方法 40只SD大鼠随机分成空白对照组、西乐葆对照组、氯丙嗪组、氯丙嗪+西乐葆组,每组10只。单次给药,24 h后采集血液测定肝脏生化指标,之后处死大鼠,取肝脏组织做病理检查以及应用免疫组织化学染色方法检测COX-2的表达。结果氯丙嗪组肝损伤明显,氯丙嗪+西乐葆组肝损伤较氯丙嗪组严重。对照组大鼠肝脏组织未见COX-2的阳性表达;氯丙嗪组有8例COX-2呈阳性表达,阳性率为80%,氯丙嗪+西乐葆组有2例COX-2呈阳性表达,阳性率为20%。结论 COX-2在氯丙嗪所致大鼠急性肝损伤肝组织中表达明显升高,阻断COX-2后肝损伤加重,COX-2表达增高可能是机体对抗氯丙嗪所致大鼠急性肝损伤的一种保护性机制。Objective To investigate the role of COX-2 in chlorpromazine-induced liver injury in rats. Methods 40 SD rats were randomly divided into 4 groups: control group, celeeoxib treated group, chlorpromazine treated group and chlorpromazine + celecoxib treated group. Each group had 10 rats and each rat was given a single dose of the appropriate drug. After 24 hours, blood was collected to perform serum biochemical test of liver function, and liver tissue was har- vested for pathological examination and COX-2 expression. Results There was obvious liver damage in chlorpromazine treated group, and liver injury was aggravated in inchlorpromazine + celecoxib treated group. There was no expression of COX-2 in hepatic tissue of control group. Intensity of COX-2 expression increased in the ehlorpromazine treated group, and decreased significantly in the presence of COX-2-selective inhibitors celecoxib. Conclusion Induction of COX-2 expression may be a protective mechanism against acute liver injury induced by ehlorpromazine.
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