Protective Effect and Mechanism of Gypenosides on Hippocampus Neurons in Rats with Chronic Cerebral Ischemia

OBJECTIVE To explore the protective effect of gypenosides on neurons of hippocampus in rats with chronic cerebral ischemia and its possible mechanism. METHODS Fifty healthy male SD rats were randomly divided into 5 groups:sham operation group, model group, gypenosides high, medium and low dose groups, 10 rats in each group. The chronic cerebral ischemia model was established by permanent ligature of bilateral common carotid artery. After 24 h of the operation, rats in gypenosides high, medium and low dose group were fed with 100, 50, 25 mg·kg^-1 gypenosides saponins respectively, and 1 times·d^-1 for 8 weeks. The Morris water maze method was used to detect the spatial learning and memory of rats; the number of neuron apoptosis in hippocampus was detected by TUNEL; the expression of GSK-3β and TNF-α protein was detected by Western blot, and the expression of apoptosis-related protein P38 and caspase-3 were detected. RESULTS Compared with the model group, the escape latency of gypenosides high, medium and low dose groups was significantly shortened(P<0.01) and the number of passing through the safety platform increased(P<0.05), the number of neuron apoptosis in the hippocampus was significantly decreased(P<0.01), the expression of GSK-3β and TNF-α protein decreased significantly(P<0.01), and the expression of P38 and caspase-3 decreased significantly(P<0.01). CONCLUSION Total glucoside of gypenosides can inhibit the expression of apoptosis-related protein P38 and caspase-3, thus protecting the neurons.