瑞芬太尼对人肝细胞缺氧复氧损伤的保护作用  

Protective effect of remifentanyl on cultured hepatocytes against injury induced by anoxia-reoxygenation

作　　者：魏勇[1] 陶国才[1] 顾健腾[1] 崔剑[1] 易斌[1] 

机构地区：[1]第三军医大学西南医院麻醉科,重庆400038

出　　处：《重庆医学》2007年第21期2191-2192,2195,共3页Chongqing medicine

摘　　要：目的探讨瑞芬太尼对人肝细胞缺氧复氧损伤的保护作用。方法人肝细胞株HL-7702,建立培养肝细胞缺氧复氧损伤模型。将培养的肝细胞分为7组,每组6个样本,缺氧培养15h,复氧5h,然后分别取上清液和肝细胞线粒体,测定ALT、AST、MDA的含量和SOD的活性。结果与正常对照组相比较,损伤对照组的ALT、AST、MDA明显升高,而SOD活性明显下降(P<0.05)。低浓度的瑞芬太尼(5、10、20ng/ml)能使细胞内ALT、AST、MDA明显降低(P<0.05)及SOD活性明显升高(P<0.05)。而瑞芬太尼浓度>30ng/ml时,其结果与损伤对照组比较差异无统计学意义。结论低浓度瑞芬太尼对缺氧复氧的肝细胞损伤具有保护作用。Objective To assess the protective effect of remifentanil on cultured human hepatocytes against injury induced by anoxia-reoxygenation. Methods A hepatocyte anoxia-reoxygenation model was established. Cultured hepatocytes were randomly divided into 7 groups： group A received no anoxia served as control; group B received 15 hours anoxia followed by 5 hours reoxygenation ; and group C, D, E, F, G received 5 ng/ml, 10ng/ml, 20ng/ml, 30ng/ml, 40ng/ml remifentanil respectively before re-oxygenation. The content of ALT, AST, MDA in the culture medium and the SOD viability in the mitochondria were measured at the end of the experiment. Results Anoxia-reoxygenation caused dramatic increase in the content of ALT,AST,MDA,and decrease in SOD viability compared with those in control group. Remifentanil 5ng/ml, 10ng/ml,and 20ng/ml significantly attenuated the increases in ALT,AST,MDA content,and enhanced SOD viability caused by anoxia-reoxygenation. Remifentanil beyond 30ng/ml did not produce any significant changes. Conclusion Low concentrative remifentanil can produce protective effects on cultured hepatocytes against anoxia-reoxygenation injury.

关 键 词：瑞芬太尼 肝细胞 缺氧 复氧 保护 

分 类 号：R96[医药卫生—药理学]