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

发布时间：2018-05-24 18:30

本文选题：高活性小牛血去蛋白提取物 + 酒精性肝损伤　；参考：《吉林大学学报(医学版)》2016年04期

【摘要】：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20mL·kg-1,低、中和高剂量DECB组小鼠分别给予0.125、0.250和0.500g·kg-1 DECB,阳性药物组小鼠给予护肝片0.63g·kg-1,每天1次,连续30d,末次给药1h后,除对照组外,其他各组小鼠一次性给予50%乙醇14mL·kg-1,并禁食16h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(P0.05),醉酒时间缩短(P0.05),中、高剂量DECB组小鼠血清ALT和AST活性均明显降低(P0.05)。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(P0.05),GSH水平明显升高(P0.05)。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。
[Abstract]:Aim: to observe the protective effect of calf blood deproteinization extract (DECB) on liver injury induced by ethanol in mice and to explore its mechanism. Methods: 60 healthy ICR mice were randomly divided into control group, model group, positive drug group and low, medium and high dose DECB groups, with 10 in each group. The mice in the control group were given normal saline 20mL kg-1, the mice in the low, middle and high dose DECB groups were given 0.125 kg-1 / kg -1 and 0.500 g kg-1 / kg, respectively, and the mice in the positive drug group were given 0.63 g / kg -1 Hugan tablet once a day for 30 days, except for the control group. Mice in other groups were given 50% ethanol 14mL kg-1 and fasting for 16 hours to establish acute alcoholic liver injury model. The alcohol tolerance time and intoxication time of mice were measured. The activities of serum alanine aminotransferase (alt) and aspartate aminotransferase (AST) were measured. The levels of triglyceride, glutathione (GSH) and malondialdehyde (MDAs) in liver tissue were measured. Pathological sections of liver tissue were examined. Results: compared with the model group, the intoxication symptoms of mice in each dose DECB group were obviously alleviated. The alcohol tolerance time of mice in high dose DECB group and positive drug group was prolonged (P 0.05), and the time of intoxication was shortened (P 0.05). The activities of serum ALT and AST in medium and high dose DECB group were all significantly decreased (P 0.05). Compared with the model group, the levels of MDA and TG in the liver tissue of the mice in the high dose DECB group and the positive drug group were significantly decreased. The liver histopathological injury induced by ethanol in high dose DECB group was significantly alleviated. Conclusion DECB can significantly improve the liver injury induced by ethanol, and the mechanism may be achieved by inhibiting oxidative stress in liver tissue.
【作者单位】：北华大学药学院微生物与生化药学教研室;
【基金】：吉林省科技厅科技创新与科技成果转化计划基金资助课题(0150312014ZX);吉林省科技厅医药产业发展基金资助课题(20140311084YY) 吉林省卫计委科研项目资助课题(2014078) 吉林省发改委科研基金资助课题(2014Y103)
【分类号】：R575

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