| Objective: To observe the protective effect of deproteinized extract of calf blood(deproteinized extract of calf blood,DECB)on chemical induced liver injury of mice,and to discuss its mechanism preliminarily.Methods:To establish two models of acute liver injury in mice,which were induced by alcohol and acute liver injury model induced by CCl4.In acute alcoholic liver injury experiment,sixty healthy ICR mice were divided into control group,model group,positive drug group,low,medium and high doses of DECB group(n=10).By intragastric administration,the mice in control group were given saline solution 20 m L·kg-1,the mice in low medium and high doses of DECB groups were administrated with 0.25,0.50,1.00g·kg-1DECB,the mice in positive drug group were administrated with 0.63g·kg-1Hugan Tables,one time everyday 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 m L·kg-1,and fasted for 16 h to establish the models of acute alcoholic 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 tissues were determined,and the pathological changes of liver tissues were detected.In CCl4-induced acute injury experiment,forty 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 m L·kg-1 by intragastric administration;the mice in DECB group were given 1g·kg-1DECB;the mice in positive drug group were administrated with 0.63g·kg-1 Hugan Tablets;once a day for 30 d.2h later 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(10m L·kg-1)mixed solution,then fasted to establish CCl4-induced acute injury models.The activities of aspartate aminotransferase(ALT)and alanine transaminase(AST)in serumof the mice in various groups were detected;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 cell was detected by TUNEL method.Results:In acute alcoholic liver injury experiment,compared with model group,DECB group obviously reduce the mice drunk symptom,DECB high dose group and positive drug group could extend mice the endurance time(P < 0.05),shortened drinking time(P < 0.05);DECB medium and high dose group ALT and AST activities in serum were significantly lower than model group(P < 0.05);compared with model group,DECB medium,high dose group and positive drug group MDA and TG levels in mice liver tissue were obviously reduced,the difference was statistically significant(P < 0.05);compared with model group,DECB high dose group mice liver tissue pathology damage caused by ethanol significantly reduce.In CCl4-induced acute injury experiment,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 increased obviously(P< 0.05);the pathological damage of liver tissue caused by CCl4 was reduced and the apoptosis index was significantly decreased.The results showed that there were 9 differently expressed genes in the apoptotic pathway.The expression of the 2 genes was up-regulated and the expression of the 7 genes was down regulated.Conclusion:DECB plays a protective role in chemical induced liver injury.It can enhance the antioxidant capacity of liver and inhibit the apoptosis of liver cells.The mechanism may be related to the regulation of apoptosis pathway gene expression. |
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