西洋参枳椇子配伍对急性酒精性肝损伤的保护作用

Protective Effect of Extract from America Ginseng and Hovenia dulcis Thunb against Acute Alcohol-induced Liver Injury in Mice

目的:研究西洋参枳椇子组合物对酒精所致小鼠急性肝损伤的预防保护作用。方法:ICR小鼠适应饲养1周后,随机分为正常组、模型组、西洋参枳椇子组合物(Ⅰ,Ⅱ,Ⅲ)组。对小鼠连续灌胃西洋参枳椇子组合物(100 mg/kg·bw)14 d后,除正常组外,其余各组均在24 h内灌胃3次酒精(5 g/kg)诱导肝损伤。末次给予酒精6 h后,处死小鼠,检测各组小鼠血清中AST、ALT活力及TG含量,检测肝脏中GSH-Px、SOD活力及GSH和MDA含量,通过H&E染色观察肝脏病理组织变化,利用蛋白印记方法检测肝组织中p-ERK、p-JNK和p-P38蛋白的表达。结果:与模型组小鼠比较,西洋参枳椇子组合物能够明显降低由急性酒精摄入引起的血清中AST、ALT活力升高(P<0.05),降低血清中TG水平(P<0.05)和肝组织中MDA含量(P<0.01),提高肝组织中抗氧化酶SOD和GSH-Px活力(P<0.01),且升高肝组织中GSH水平(P<0.01)。病理切片观察表明,模型组以出现脂肪滴为变性为主,部分出现炎性细胞浸润,各给药组对小鼠肝脏病理变化有不同程度改善作用,西洋参枳椇子组合物极显著抑制p-ERK、p-JNK和p-P38表达(P<0.01),抑制肝细胞凋亡。结论:西洋参枳椇子组合物对急性酒精诱导的小鼠肝损伤具有较好的预防保护作用。

Objective: To study the preventive effects of American ginseng and Hovenia dulcis Thunb(AGH) on alcoholinduced acute liver injury in mice. Methods: After one week of adaptation, ICR mice were randomly divided into normal group, model group and AGH(Ⅰ,Ⅱ,Ⅲ) groups. After giving the mice a continuous intragastric administration of AGH(100 mg/kg·bw) for 14 days, all groups except the normal group were given three times of alcohol(5 g/kg) within 24 hours to induce liver damage. After the third alcohol administration for 6 hours, the mice were sacrificed. The activities of Aspartate aminotransferase(AST), Alanine aminotransferase(ALT) and the content of Triglycerides(TG) in serum were tested. The activity of Glutathione peroxidase(GSH-Px), Superoxide dismutase(SOD) and the contents of Glutathione(GSH) and Malondialdehyde(MDA) were detected. Pathological changes of liver were observed by H & E staining. The expression of p-ERK, p-JNK and p-P38 protein in liver tissue was detected by WB method. Results: Compared with model group, AGH could significantly reduce the activities of AST and ALT in serum(P<0.05), decreased the level of TG in serum(P<0.05) and MDA content in liver tissue(P<0.01). Meanwhile, AGH could also increase the activities of SOD and GSH-Px in liver tissue(P<0.01) and improve the level of GSH in liver tissue(P<0.01). Pathological observation showed that the main degeneration was fat drops, and some inflammatory cells were infiltrated in model group. AGH group had different degree of improvement on the pathological changes of the liver in mice. AGH significantly inhibited the expression of p-ERK, p-JNK and p-P38(P<0.01) and inhibited the apoptosis of hepatocytes. Conclusion: AGH has obvious protective effect on acute alcohol-induced liver injury in mice.