Effect of Gly14-Humanin on Neuroprotectant and Free Radicals Metabolism in Rats of Focal Cerebral Ischemia Reperfusion Injury

OBJECTIVE To study the effect ofGly14-Humanin(HNG) on neuroprotectant and free radicals metabolism in rats of focal cerebral ischemia reperfusion injury. METHODS Ninety-six healthy male Sprague-Dawley rats were randomly divided into sham-operation group, model group, normal saline group and HNG group, with 24 rats in each group. Rat model of acute middle cerebral artery occlusion (MCAO) and reperfusion was established by suture embolism, relevant medicines (normal saline in the rats of the sham-operation group and normal saline group, HNG in the rats of the HNG group) were given to rats 5 days before operation respectively(iv, five times, qd). After cerebral ischemia 4.5 h and 24 h of reperfusion, neurological deficit score(NDS), brain water content, detect the activitiy of SOD, levels of GSH and MDA in cerebral tissue, HE staining was used to observe morphologic changes of neuron cells in ischemia region, TUNEL staining was used to detect the number of neuron apoptosis were penformed for each group. Then the linear correlation analysis was used to determine the assocination between the levels of GSH and neuron apoptosis in cerebral tissue with HNG group. RESULTS Compared with sham-operation group, the NDS, the brain water content, the activitiy of SOD and levels of GSH were significantly decreased, but the levels of MDA and number of neurocytes apoptosis were significantly increased in the other three groups(P<0.01). Compared with normal saline group and model group, the NDS, the brain water content, the activitiy of sod and levels of GSH were significantly increased, but the levels of MDA and number of neurocytes apoptosis were significantly decreased in HNG group(P<0.05). The number of neurons and levels of GSH in HNG group were perfect positive correlations(r=0.462, P<0.001). CONCLUSION Gly14-Humanin can mitigate the neurologic deficit. Its mechanism is probably related to lighten the brain water content, increase the activitiy of SOD and levels of GSH, resistance focal cerebral ischemia reperfusion injury, decrease the neuro apoptosis of ischemic area.