高活性小牛血去蛋白提取物对小鼠酒精性肝损伤的保护作用

摘要

Objective:To observe the protective effect of deproteinized extract of calf blood (DECB)on the ethanol-induced liver injury of the mice,and to preliminaryly discuss its mechanism. Methods:Sixty healthy ICR mice were divided into control group,model group,positive drug group,low,medium and high doses of DECB groups (n=10).By intragastric administration,the mice in control group were given 20 mL·kg-1 saline solution, the mice in low,medium and high doses of DECB groups were administrated with 0.125,0.250,0.500 g·kg -1 DECB,and the mice in positive drug group were administrated with 0.63 g·kg -1 Hugan Tablets;once a day for 30 d. 1 h after the last administration,except control group,the mice in other groups were administrated with one-time grant of 50% ethanol 14 mL·kg -1 ,and fasted for 16 h to establish the models of acute alcohol liver injury.The endurance alcohol time and drunk time of the mice were determined,the activities of aspartate aminotransferase (ALT)and alanine transaminase (AST)activity in serum of the mice were detected,the levels of triglyceride (TG),glutathione (GSH)and malonic dialdehyde (MDA)in liver tissue were determined,and the pathological changes of liver tissue were detected.Results:Compared with model group,the drunk symptoms of the mice in different doses of DECB groups were obviously reduced,the endurance time of the mice in high dose of DECB group and positive drug group was prolonged (P <0.05),and the drinking time was shortened (P <0.05);the ALT and AST activities in serum in mediun and high doses of DECB groups were significantly lower than those in model group (P <0.05).Compared with model group,the MDA and TG levels in liver tissue of the mice in medium and high doses of DECB groups and positive drug group were obviously reduced,and the GSH levels were increased (P <0.05);compared with model group,the pathological damages of liver tissue of the mice in high dose of DECB group caused by ethanol were significantly reduced.Conclusion:DECB can improve ethanol-induced liver injury which may be related to the inhibition of hepatic oxidative stress response.%目的：观察小牛血去蛋白提取物（DECB）对乙醇所致小鼠肝损伤的保护作用，并初步探讨其作用机制。方法：健康 ICR 小鼠60只，随机分为对照组、模型组、阳性药物组和低、中、高剂量 DECB 组，每组10只。腹腔灌胃给药，对照组小鼠给予生理盐水20 mL·kg －1，低、中和高剂量 DECB 组小鼠分别给予0.125、0.250和0.500 g·kg－1 DECB，阳性药物组小鼠给予护肝片0.63 g·kg －1，每天1次，连续30 d，末次给药1 h后，除对照组外，其他各组小鼠一次性给予50％乙醇14 mL·kg －1，并禁食16 h 建立急性酒精性肝损伤模型。测定小鼠的耐受酒精时间和醉酒时间，检测血清丙氨酸氨基转移酶（ALT）和天冬氨酸氨基转移酶（AST）活性，检测肝组织中甘油三酯（TG）、谷胱甘肽（GSH）和丙二醛（MDA）水平，并进行肝组织病理切片检查。结果：与模型组比较，各剂量 DECB 组小鼠醉酒症状明显减轻，高剂量 DECB 组和阳性药组小鼠酒精耐受时间延长（P ＜0.05），醉酒时间缩短（P ＜0.05），中、高剂量 DECB 组小鼠血清 ALT 和 AST 活性均明显降低（P ＜0.05）。与模型组比较，中、高剂量 DECB 组和阳性药物组小鼠肝组织中 MDA 和 TG 水平明显降低（P ＜0.05），GSH 水平明显升高（P ＜0.05）。高剂量 DECB 组小鼠乙醇所致肝组织病理学损伤明显减轻。结论：DECB能明显改善乙醇所致肝损伤，其机制可能是通过抑制肝组织氧化应激反应实现的。