竹节参提取物对小鼠急性酒精性肝损伤的保护作用

目的 研究竹节参60%乙醇提取物对小鼠急性酒精性肝损伤的保护作用。方法 将40只昆明种小鼠随机分为正常组、模型组、竹节参提取物高剂量组、竹节参提取物低剂量组、水飞蓟宾组;采用白酒灌胃的方式建立小鼠急性酒精性肝损伤模型。测定各组小鼠ALT、AST、TG含量水平,以及肝组织超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性,丙二醛(MDA)含量,光学显微镜观察小鼠肝脏病理变化,PCR技术检测SOD₁和GPX₁基因表达水平。结果 与正常组相比较,模型组小鼠肝脏出现明显脂肪变性,血清ALT、AST和TG的水平升高,肝脏SOD 和GSH-Px活性明显降低,同时MDA含量显著升高,差异具有统计学意义(P<0.05 或P<0.01);与模型组相比,竹节参提取物高、低剂量组和水飞蓟宾组均可降低ALT、AST和TG的含量;升高肝脏SOD和GSH-Px活性,同时降低MDA的含量;并且肝组织SOD₁和GPX₁基因的表达水平明显上调,差异具有统计学意义(P<0.05 或P<0.01)。结论 竹节参提取物对小鼠急性酒精性肝损伤有明显的保护作用,其机制可能是通过上调SOD₁和GPX₁的基因表达,从而减轻酒精诱导的氧化应激对肝脏的损伤。

Protection of Panax Japonicus extract against acute alcoholic liver injury in mice

AIM: To investigate the protective effects of Panax Japonicus extract(PJE)on ethanol-induced liver injury in mice. METHODS: KM mice were randomly divided into five groups as below: normal control group,model group, PJE high-dose group, PJE low-dose group and silybin group. The levels of serum alanine aminotransferase(ALT), aspartate aminotransferase(AST), and triglyceride(TG)were assayed.The activity of liver Superoxide Dismutase(SOD), Glutathione Peroxidase(GSH-Px) and malondialdehyde(MDA)content were measured, and liver histopathology was also examined. Polymerase Chain Reaction (PCR) was applied to detect the mRNA expression of SOD₁ and GPX₁ gene. RESULTS: Compared with normal control group, the liver dysfunction and hepatic tissue damage as well as enhancement of lipid peroxidation in the model group,and the levels of ALT,AST,AST in serum were increased,the activity of SOD and GSH-Px in liver were decreased,and the content of MDA was increased,there were statistical difference (P<0.05 or P<0.01). Compared with the model group,the serum levels of ALT, AST and TG were decreased in the PJE high-dose group, PJE low-dose group and silybin group, and the activity of SOD and GSH-Px in liver were increased,the content of MDA was decreased;Moreover, the mRNA expressions of SOD₁ and GPX₁ in liver tissue increased marketly, there were statistical difference (P<0.05 or P<0.01).CONCLUSION: PJE has obvious protective effects on acute alcoholic liver injury in mice via attenuating hepatic lipid peroxidation,and the mechanism maybe up-regulate the mRNA expression of SOD₁ and GPX₁ gene.