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Protective Effects of Chrysophanol on Liver Injury Induced by Cerebral Ischemia-Reperfusion in Mice
ZHAO Wei, LI Fang-jiang, WANG Shu
2014, 4 (4):
1-9.
Objective: To research the protective effects of chrysophanol(Chry) on liver injury induced by cerebral ischemia-reperfusion in mice and its molecular preliminary mechanism. Methods: By improved Himori method, Cerebral ischemia-reperfusion injury model of mice was produced in conscious mice by temporarily obstructing bilateral common carotid arteries. The mice were randomly divided into six groups: control group, sham-operated group, model group, chrysophanol group (10.0, 1.0, 0.1mg·kg-1). The alanine aminotransferase(ALT), aspartate transaminase(AST), superoxide dismutase(SOD) and malondialdehyde(MDA) in the plasma and the SOD and MDA in the liver were measured with biochemical methods in mice. The expression of Caspase3 was determined by immunohistochemistry, and the expression of Caspase3 mRNA was detected using in situ hybridization assay. Results: There are no obvious pathological changes in various indicators between control group and sham-operated group. For mice of modle group, the concentration of ALT, AST, MDA increased and the activity of SOD decreaed in plasma; the concentration of MDA increased and the activity of SOD decreaed in liver; the expression of Caspase3 and Caspase3 mRNA strengthened in liver. For mice of chrysophanol group, chrysophanol(10.0, 1.0, 0.1 mg·kg-1) could decrease the concentration of ALT, AST, MDA and increase the activity of SOD in plasma; chrysophanol(10.0, 1.0, 0.1 mg·kg-1) could decrease the concentration of MDA and increase the activity of SOD in liver; and chrysophanol(10.0, 1.0, 0.1 mg·kg-1) could attenuate the expression of Caspase3 and Caspase3 mRNA in liver. Conclusions: Cerebral ischemia-reperfusion may cause liver damage secondarily. Chrysophanol showed the protective effects on injury liver in mice with cerebral-schemia reperfusion injury, perhaps the mechanism is involved in attenuating the expression of Caspase3 and Caspase3 mRNA, then inhibiting the cell apoptosis, enhancing the ability of the antioxidative stress.
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