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环氧合酶-2及肝细胞凋亡在非酒精性脂肪性肝炎中的作用 被引量:2

The role of cyclooxygenase-2 and hepatocyte apoptosis in the pathogenesis of nonalcoholic steatohepatitis
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摘要 目的探讨环氧合酶(COX)-2及肝细胞凋亡在非酒精性脂肪性肝炎(NASH)发生中的作用。方法雄性SD大鼠30只,随机分为模型组、乙醇灌胃对照组和正常对照组,每组各10只。模型组给予高脂饮食(普通饲料基础上加10%猪油、2%胆固醇和5%蛋黄粉)。乙醇灌胃对照组在普通饲料中加乙醇灌胃喂养。正常对照组给予普通饲料。动物喂养12周后处死并取肝脏组织,用免疫组化法及逆转录(RT)-PCR法检测COX-2表达,TUNEL法观察肝细胞凋亡。结果模型组(0.97±0.32)和乙醇对照组(0.89±0.19)大鼠COX-2表达水平均明显高于正常对照组(0),差异有统计学意义(P<0.01)。模型组(3.26±0.90)和乙醇对照组(3.33±0.78)的肝细胞凋亡指数明显高于正常对照组(0.80±0.65),差异亦有统计学意义(P<0.01)。模型组与乙醇对照组之间COX-2表达和肝细胞凋亡指数差异均无统计学意义(P>0.05)。结论COX-2在NASH发生中发挥着重要作用,肝细胞凋亡是NASH发生的重要机制。 Objective To investigate the role of cyclooxygenase(COX)-2 and hepatocyte apoptosis in the pathogenesis of nonalcoholic steatoheptatitis (NASH) . Methods Thirty male SD rats were divided randomly into three groups. The rats in NASH group (n= 10) were fed with high fatty diet, the rats in alcoholic steatoheptatitis (ASH) group (n= 10) were fed with standard diet with alcohol oral layage, and the rats in control group(n=10) were fed with standard diet for 12 weeks. Hepatic COX-2 expression was determined by RT-PCR and immunohistochemistry. Hepatocyte apoptosis was determined by TUNEL assay. Results The mRNA expression of COX-2 and hepatocyte apoptosis were significant higher in NASH group (0.97±0. 32 and 3. 26±0.90, respectively) and ASH group (0.89±0. 19 and 3.33±0. 78, respectively) than those in control group(0 and 0. 80±0. 65, respectively, P〈0. 01). There was no significant difference of COX-2 expression and hepatocyte apoptosis between NASH group and ASH group (P〉0. 05) . Conclusion COX-2 may play an important role in the pathogenesis of NASH. The hepatocyte apoptosis is an important mechanism of NASH pathogenesis.
出处 《中华消化杂志》 CAS CSCD 北大核心 2007年第5期326-329,共4页 Chinese Journal of Digestion
基金 上海市高校青年基金(SJW0101)
关键词 脂肪肝 环氧合酶2 肝细胞 凋亡 Fatty live Cyclooxygenase 2 Hepatocytes Apoptosis
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  • 1Angulo P, Keach JC, Batts KP, et al. Independent predictors of liver fibrosis in patients with nonalcoholic steatohepatitis. Hepatology, 1999, 30:1356-1362.
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