目的:研究人参枳椇子提取物对酒精所致小鼠急性肝损伤的保护作用。方法:不同配伍比例的人参枳椇子提取物以100 mg/kg的剂量连续灌胃小鼠3 d后,除正常组外,其余各组小鼠给予体积分数为50%的乙醇(6 g/kg·bw)灌胃,建立一次性暴饮小鼠急性酒精性肝损伤模型。在给予酒精12 h后处死小鼠,检测各组小鼠血清中天冬氨酸氨基转移酶(Aspartate aminotransferase,AST)、丙氨酸氨基转移酶(Alanine aminotransferase,ALT)的活力及甘油三酯(Triglyceride,TG)、高密度脂蛋白胆固醇(High-density lipoproteins,HDL-C)、低密度脂蛋白胆固醇(Low-density lipoproteins,LDL-C)的含量,肝脏中谷胱甘肽过氧化物酶(Glutathione peroxidase,GSH-Px)、超氧化物歧化酶(Superoxide dismutase,SOD)的活力及还原型谷胱甘肽(Glutathione,GSH)、丙二醛(Malondialdehyde,MDA)含量。利用酶联免疫吸附法测定血清中肿瘤坏死因子α(TNF-α)、白介素-1β(IL-1β)的含量变化,并用反转录PCR法检测TNF-α和IL-1β的基因表达水平。结果:与模型组小鼠比较,人参枳椇子提取物能够明显降低由急性酒精摄入引起的血清中AST、ALT活力的升高(p<0.05);降低血清中TG、LDL-C的含量(p<0.05),升高HDL-C的水平(p<0.05),改善脂质代谢失衡;提高肝组织中抗氧化酶SOD和GSH-Px的活力(p<0.05),减少肝组织中GSH损耗并抑制肝组织中MDA含量增加(p<0.05),提高抗氧化能力保护肝脏损伤;下调炎症因子TNF-α、IL-1β的表达来减轻炎症损伤(p<0.05)。结论:人参枳椇子提取物对急性酒精诱导的小鼠肝损伤有明显的保护作用。
The potential protective effects of water extract from Panax ginseng and Hovenia dulcis Thunb (PHE) on mice with alcohol-induced liver injury were evaluated in this paper. METHODS:PHE, which obtained by different compatibility ratio of Panax ginseng and Hovenia dulcis Thunb, were gavaged to mice with at a dose of 100 mg/kg for 3 d. Acute liver injury was established by gavage of 50% ethanol. After oral administration of content of alcohol for 12 h, the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), triglyceride (TG), high-density lipoproteins (HDL-C) and low-density (LDL-C) in serum, as well as the activities of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), glutathione (GSH) and malondialdehyde (MDA) in liver were measured. The levels of TNF-α and IL-1β in the serum were measured by enzyme-linked immunosorbent assay (ELISA) and the mRNA expressions of TNF-α and IL-1β in liver tissure were detected by reverse transcription polymerase chain reaction (RT-PCR). RESULTS:As Compared with the model group, PHE could significantly reduce the activities of AST and ALT in serum. PHE could significantly inhibit the imbalance of lipid metabolism by reducing the content of serum TG and LDL-C (p<0.05) and increasing the level of HDL-C (p<0.05). Meanwhile, PHE could also improve antioxidant capability against liver injury by enhancing the activities of SOD and GSH-Px (p<0.05), increasing the level of GSH and decreasing the content of MDA in liver tissue (p<0.05). PHE adjusted the inflammatory response through decreasing the level of TNF-α and IL-1β (p<0.05). Conclusion:PHE indicated obvious protective effect on mice with acute alcohol-induced liver injury in mice.