摘要

In the present study, we have investigated the neuroprotective potential of ginsenoside Re (Re) in the middle cerebral artery occlusion model in Sprague-Dawley rats. Adult male Sprague-Dawley rats were treated with Re (5, 10 or 20mgkg-1, P.O. for 7 days, once a day) prior to occlusion. There was a significant increase in the neurological symptoms in ischemic animals as compared with the sham group animals. These effects were attenuated by 10 and 20 mg kg(-1) Re, P.O. There was a significant increase in the level of malondialdehyde (MDA) in ischemic animals indicating oxidative stress. An elevated level of MDA in ischemic animals was reduced by 10 and 20 mg kg(-1) Re, P.O., respectively. It was observed that Re significantly decreased mitochondrial swelling, thereby preventing the reduction of H+-ATPase activity. This study demonstrates the neuroprotective potential of Re in cerebral ischemia-reperfusion injury in rats.