Neuroprotection of total steroid saponins from Dioscorea zingiberensis C.H.Wright against transient focal cerebral ischemia-reperfusion injury in rats via its anti-inflammatory and anti-apoptotic effects

OBJECTIVE The total steroid saponins(TSSN)isolated from Dioscorea zingiberensis C.H.Wright(D.zingiberensis)has shown a variety of beneficial bioactivities.However,there are no reports about the neuroprotective effects of the TSSN until now.Therefore,we explored the neuroprotective effects of TSSN on rats against transient focal cerebral ischemia-reperfusion(I/R)and the underlying mechanisms.METHODS The healthy adult Sprague-Dawley rats were randomly assigned into six groups.After pre-treatment with the TSSN intragastrically for six days,the rats were subjected to the ischemia injury by the surgery of middle cerebral artery occlusion(MCAO)for 90 min.Some indexes were evaluated and detected.RESULTS As compared to the I/R group,TSSN group of rats,especially given the 30 mg·kg^-1 of TSSN,not only marked reduction in the neurological deficit scores,cerebral infarct volume,and brain edema,but also an increase in neuron survival(Nissl bodies)in the hippocampal cornuammons 1(CA1)and cortex hemisphere of the ipsilateral ischemia.At the same time,the inflammatory cytokines in serum induced by MCAO were significantly alleviated by the TSSN pre-administration.What′s more,the increase of caspase-3 was evidently reduced in the CA1 and cortex of the hemisphere injured brain.Finally,the down-regulating anti-apoptotic Bcl-2 and up-regulating pro-apoptotic Bax proteins were obviously suppressed.CONCLUSION TSSN plays a potential neuroprotective role against a severe injury induced by transient focal cerebral ischemic reperfusion in a rat experimental model,and this role may be mediated by its antiinflammatory and anti-apoptotic actions.

OBJECTIVE The total steroid saponins（TSSN） isolated from Dioscorea zingiberensis C. H. Wright（D.zingiberensis） has shown a variety of beneficial bioactivities. However, there are no reports about the neuroprotective effects of the TSSN until now. Therefore, we explored the neuroprotective effects of TSSN on rats against transient focal cerebral ischemia-reperfusion（I/R） and the underlying mechanisms. METHODS The healthy adult Sprague-Dawley rats were randomly assigned into six groups. After pre-treatment with the TSSN intragastrically for six days, the rats were subjected to the ischemia injury by the surgery of middle cerebral artery occlusion（MCAO） for 90 min. Some indexes were evaluated and detected. RESULTS As compared to the I/R group, TSSN group of rats, especial y given the 30 mg·kg-1 of TSSN, not only marked reduction in the neurological deficit scores, cerebral infarct volume, and brain edema, but also an increase in neuron survival（Nissl bodies） in the hippocampal cornuammons 1（CA1） and cortex hemisphere of the ipsilateral ischemia. At the same time, the inflammatory cytokines in serum induced by MCAO were significantly alleviated by the TSSN pre-administration. What′s more, the increase of caspase-3 was evidently reduced in the CA1 and cortex of the hemisphere injured brain. Final y, the down-regulating anti-apoptotic Bcl-2 and up-regulating pro-apoptotic Bax proteins were obviously suppressed. CONCLUSION TSSN plays a potential neuroprotective role against a severe injury induced by transient focal cerebral ischemic reperfusion in a rat experimental model, and this role may be mediated by its antiinflammatory and anti-apoptotic actions.