松果菊苷在肝脏缺血再灌注损伤中的保护作用及机制研究

Protective effect of echinacoside on hepatic ischemia reperfusion injury and its mechanism

目的探讨松果菊苷预处理对大鼠肝脏缺血再灌注损伤的保护作用及机制。方法SD大鼠40只随机分为假手术组、模型组、松果菊苷低、高浓度治疗组,模型组、松果菊苷低、高浓度治疗组采用阻断部分肝血供的方法建立肝脏缺血再灌注损伤模型。HE染色观察肝组织病理学变化;试剂盒测定丙二醛(MDA)活性及超氧化物歧化酶(SOD)水平;酶联免疫吸附实验分析丙氨酸氨基转移酶(ALT)及天门冬氨酸氨基转移酶(AST)含量;免疫印迹法分析HO-1、Nrf-2蛋白的表达含量。结果HE结果显示,松果菊苷低、高浓度组肝损伤程度较模型组明显改善;与模型组比较,松果菊苷低、高浓度组大鼠肝脏组织中MDA含量下降,SOD活性升高,差异均有统计学意义(P<0.05);松果菊苷低、高浓度组大鼠ALT及AST活性下降,差异均有统计学意义(P<0.05);免疫印迹法结果显示,松果菊苷治疗组HO-1、Nrf-2蛋白的表达升高,与模型组比较差异有统计学意义(P<0.05)。结论松果菊苷可以通过激活Nrf-2信号通路减轻大鼠肝脏缺血再灌注损伤。

Objective To investigate the protective effect of echinacoside on hepatic ischemia-reperfusion injury in rats and its mechanism.Methods Forty SD rats were randomly divided into sham operation group,model group,echinacoside low and high concentration treatment group.The model group,echinacoside low and high concentration treatment group were established by blocking partial hepatic blood supply.HE staining was used to observe the pathological changes of liver tissue;The activity of malondialdehyde(MDA)and the level of superoxide dismutase(SOD)were measured;The content of alanine aminotransferase(ALT)and aspartate aminotransferase(AST)was analyzed by ELISA;The protein expression levels of HO-1 and Nrf-2 were analyzed by Western blot.Results HE results showed that the liver injury degree of echinacoside low and high concentration treatment group were significantly improved than that of the model group;Compared with the model group,MDA content and SOD activity were significantly increased in the liver of the rats in echinacoside low and high concentration treatment group(P<0.05);ALT and AST activities of the rats in echinacoside low and high concentration treatment group were significantly lower(P<0.05),the differences were statistically significant(P<0.05);Western blot showed that the expression of HO-1 and Nrf-2 in echinacoside low and high concentration treatment group were significantly higher than that in model group(P<0.05).Conclusion Echinacoside could reduce liver ischemia-reperfusion injury by activating Nrf-2 signaling pathway.