Study on the intervention effect of Qileng decoction (芪棱汤) on mitochondria mediated and caspase-9 dependent apoptopic pathway / 中国中西医结合急救杂志

ABSTRACT

Objective: To evaluate the effects and partly mechanism of Qileng decoction(QLD,芪棱汤) resisting focal cerebral ischemia/reperfusion(I/R) injury in rats by apoptosis and signal transduction pathway.Methods: The rats were randomly divided into three groups including sham operation group,normal saline(NS) control group and QLD group.The model of focal cerebral I/R injury was induced by using modified thread embolizing in rats.Rats were evaluated by neurologic function score at 2 hours after ischemia and 2,4,6,12,24 and 48 hours after cerebral reperfusion,and the pathological changes of nerve cells and mitochondria ultrastructure at pallium and hippocampus CA1 region were observed at 24 hours after reperfusion.Immunohistochemical method was performed to examine the expression of cytochrome C(cyt C) and caspase-9 at different time points after reperfusion.Apoptosis of nerve cells in ischemic penumbra(IP) was also characterized by terminal deoxynucleotidyl-transferase mediated dUTP-biotin nick end labeling(TUNEL) method.Results: Compared with NS control group,neurologic function scores at different reperfusion time points were improved and the pathological changes were ameliorated at 24 hours after cerebral I/R in QLD group.Mitochondria hydropsia was alleviated,mitochondrial cristae fragmentation and granulum basale shedding were diminished,and mitochondrial basical morphology was retained.Meanwhile,apoptosis index(AI) was decreased and the expressions of cyt C and caspase-9 were reduced in IP in QLD group.Conclusion: QLD intervenes in mitochondria mediated and caspase-9 dependent apoptopic pathway.QLD lowers AI and plays a role of protecting nerve by maintaining mitochondrial basical form,stabilizing mitochondrial membrane and inhibiting the release of cyt C and activation of caspase-9.The above actions are possibly some parts of mechanisms of QLD resisting focal cerebral I/R injury.