高活性小牛血去蛋白提取物对四氯化碳致急性肝损伤模型小鼠的保护作用

Protective effect of high activity deproteinized extract of calf blood on CCl_4-induced acute liver injury of mice

目的:观察小牛血去蛋白提取物(DECB)对四氯化碳(CCl_4)所致肝损伤小鼠的保护作用,初步探讨其作用机制。方法:健康ICR种小鼠40只,随机分组法分为对照组、模型组、DECB组和阳性药物组,每组10只。各组小鼠腹腔灌胃给药,对照组和模型组小鼠给予生理盐水20mL·kg^(-1),DECB组小鼠给予DECB1g·kg^(-1),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2h后,对照组小鼠腹腔注射调和油溶液,其余各组小鼠腹腔注射10%CCl_4调和油溶液(10mL·kg^(-1))并禁食,建立CCl_4致急性肝损伤模型。测定各组小鼠血清中丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)活性和肝组织总超氧化物歧化酶(T-SOD)、谷胱甘肽(GSH)及丙二醛(MDA)水平;HE染色法观察小鼠肝组织病理表现;TUNEL方法检测小鼠肝细胞凋亡。结果:与模型组比较,DECB组和阳性药物组小鼠血清中ALT和AST活性及肝组织中MDA和GSH水平明显降低(P<0.05),T-SOD水平明显升高(P<0.05);与模型组比较,DECB组和阳性药物组小鼠肝组织病理学损伤明显减轻,凋亡细胞数明显减少。结论:DECB对CCl_4诱导急性肝损伤小鼠具有保护作用,可以增强肝脏抗氧化能力,抑制肝细胞凋亡,其机制可能与减少氧自由基和抑制脂质过氧化有关。

Objective： To observe the protective effect of deproteinized extract of calf blood （DECB） on CCl4-induced liver injury of the mice,and to preliminarily discuss its mechanism.Methods： Fourty healthy ICR mice were randomly divided into control group,model group,positive drug group, and DECB group（n=10）.The mice in control group were given saline solution 20 mL·kg-1 by intragastric administration;the mice in DECB group were given DECB 1 g·kg-1;the mice in positive drug group were administrated with Hugan Tablets0.63 g·kg-1;once a day for 30d. 2h after the last administration,the mice in control group were intraperitoneally injected with mixed solution,and the mice in other groups were intraperitoneally injected with 10% CCl4 （10 mL·kg-1） mixed solution,then fasted to estabish CCl4-induced acute injury models. The activities of aspartate aminotransferase （ALT） and alanine transaminase （AST） in serum of the mice in various groups were detected;the levels of total superoxide dismutase （T-SOD）,glutathione （GSH） and malonic dialdehyde （MDA） in liver tissue of the mice in various groups were determined. The pathological changes of liver tissue were detected by HE staining and the apoptosis of liver tissue was detected by TUNEL method.Results： The ALT and AST activities in serum of the mice in DECB group were significantly lower than those in model group （P〈0.05）;compared with model group the MDA and GSH levels in liver tissue of the mice in DECB group were reduced（P〈0.05）,the T-SOD level was obviously increased（P〈0.05）;the pathological damage of liver tissue caused by CCl4 was reduced and the apoptosis index was significantly decreased.Conclusion： DECB plays a protective role in CCl4 -induced liver injury.It can enhance the antioxidant capacity of liver and inhibit the apoptosis of liver cells.The mechanism may be related to reducing the oxygen free radicals and inhibiting the lipid peroxidation.