摘要
目的 探讨氧自由基在肝脏保存再灌注损伤 (hepaticpreservationreperfusioninjury ,HPRI)中的作用及丹参的保护作用。方法 建立大鼠肝脏保存再灌注模型 ,分别检测肝脏保存 0、8、1 6、2 4、32h组在不同灌注时间点组织超氧化物歧化酶 (SOD)、丙二醛 (MDA)和灌注液谷草转氨酸(AST)的变化 ,并观察肝细胞形态学的改变。结果 与正常组 (保存 0h组 )比较 ,保存 1 6、2 4、32h组不同再灌注时点SOD显著降低 (P <0 .0 5) ,而MDA和AST均明显升高 (P <0 .0 5) ,肝细胞形态也发生异常改变 ;应用丹参组 ,SOD则明显升高 ,MDA和AST明显下降 ,与对照组比较 ,差异均有显著性(P <0 .0 5)。结论 氧自由基是导致HPRI的重要因素 ,丹参能清除氧自由基 。
Objective\ To explore the role of oxygen free radicals (OFR) in hepatic preservation reperfusion injury (HPRI) of rats and the protective effect of salviamiltiorrhiza (SM). Methods\ The model of the preservation reperfusion of isolated rat liver was established. The changes of superoxide dismutase (SOD) and malondialdehyde (MDA) in the liver and aspartate aminotransferase (AST) in perfusion fluid were studied at different preservation reperfusion time points (0,8,16,24,32 h), and morphological changes of hepatocytes were observed. Results\ The activity of SOD was decreased ( P <0.05) and MDA and AST levels increased significantly ( P <0.05) at the liver preservation reperfusion points of 16, 24 and 32 h as compared with those of normal group. Abnormal changes of hepatocytes were found in morphology. After the administration of SM, SOD was obviously increased, and MDA and AST significantly decreased as compared with those in control group ( P <0.05). Conclusion\ OFR may be one of the primary causes for HPRI. SM can attenuate HPRI by eliminating OFR.\;
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2000年第3期237-238,共2页
Chinese Journal of Experimental Surgery
关键词
氧自由基
肝脏保存
再灌注损伤
丹参
HPRI
Oxygen free radicals
\ Liver
\ Preservation reperfusion injury
\ Salviamiltiorrhiza
