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The first part of the rat after focal cerebral ischemia NR2B, endo G expression changes Objective: To observe the N-methyl-D aspartate receptor subunit NR2B protein and apoptosis inducing factor endonuclease G (endonuclease G, endo G) in focal cerebral ischemia reperfusion brain expression of the basal ganglia, and the infarct volume and neuronal apoptosis were studied. Investigate cerebral ischemia-reperfusion injury mechanism of nerve cells. Methods: 63 weighing 250 to 300 g healthy male adult Wistar rats were randomly divided into normal group (A), sham group (B), 1h cerebral ischemia-reperfusion group (C), select \middle cerebral artery occlusion (MCAO) model, using immunohistochemistry and image analysis methods observed one hour after focal cerebral ischemia and reperfusion 6, 24 and 72h after the basal ganglia and the endo G NR2B expression, TTC France determination of infarct volume, TUNEL method for the determination neuronal apoptosis. Results: cerebral ischemia and reperfusion can cause ischemic neuronal necrosis or apoptosis, infarct volume compared with the normal group and sham group significantly increased number of apoptotic cells at 24h reperfusion peaked and appeared in the cells around the necrotic area This positive expression in endo G laws are virtually identical: ischemia / reperfusion 1h, NR2B receptor expression decreased with cerebral ischemia / reperfusion time prolonged, NR2B positive expression was gradually increased, 6h after reperfusion and reached its peak, thereafter declined sharply, continuing until 72h after; ischemia / reperfusion 1h, endo G protein expression began to increase, with cerebral ischemia / reperfusion time prolonged, NR2B positive expression and gradually increased after reperfusion and peaked at 24h, thereafter gradually decreased, continuing until after 72h. Conclusion: NR2B in ischemic brain injury in rats showed early in the ischemic reduction - increase - a further reduction of the dynamic process of change; endo G expression is elevated in the early stage of ischemia, followed by a sharp decrease expression pattern showed a time-dependent manner. Cerebral ischemia can cause ischemic neuronal necrosis or apoptosis. The second part ifenprodil tartrate, ginsenoside-Rd and their combination on cerebral ischemia-reperfusion injury in rats Objective ifenprodil tartrate, ginsenoside-Rd and combined neuroprotective effect. Methods Male adult Wistar rats 117 randomly divided into normal group, model group, tartaric Ifenprodil group ginsenoside-Rd group and the combination group. Ifenprodil tartrate tartrate group to Ifenprodil 2mg/Kg, preparation of appropriate concentration solution; ginsenoside-Rd group to ginsenoside-Rd 2mag/Kg, temporary use when formulated into a solution of appropriate concentration; while giving the combined group Both drugs intervention. Intraperitoneal injection, 1 times / day for 3 consecutive days, the first four days of modeling, modeling success and by the score into the group continue after therapeutic intervention in cerebral ischemia reperfusion 1h 1h, 6h, 24h, 72h were sacrificed, rats in each group detected neurological deficit score, infarct ratio, HE staining, the number of neuronal apoptosis and immunohistochemical NR2B, endo G expression changes. 1) neurological function: Compared with model group, at 24h after reperfusion, ginsenoside-Rd group score difference was statistically significant (P <0.05), the combined treatment group score difference was significant (P <0.01 ); other point in time the drug group compared with the model group showed no significant difference (P> 0.05). 2) at 24h reperfusion cerebral infarction than changes in the drug group compared with the control group infarct, there was significant difference (P <0.01). 3) Compared with model group, treatment group in cerebral ischemia-reperfusion 6h, 24h, 72h can significantly reduce the positive expression of apoptotic cells (P <0.01), drug group comparison between groups, the combined treatment group can significantly reduce the withered nerve cells death (P <0.01). 4) HE staining: drug group compared with the control group, model group decreased nerve cells, nerve cell body reduced residual deformation karyopycnosis stained nucleolus, heterochromatin disappeared, interstitial edema. Most drug intervention group compared with intact neuronal structures, form relatively normal, mild interstitial edema. 5) on the NR2B expression: Compared with model group, reperfusion 6h, medication alone group and the combined group could significantly reduce ischemia-reperfusion injury in rat basal ganglia ischemic area NR2B protein expression (P <0.01 ), but the combination therapy group than medication alone group decreased more significantly. 7) on the endo G expression: Compared with model group, in ischemia-reperfusion 6h, 24h, 72h, medication alone group and combination group can reduce endoG positive expression, the difference was statistically significant (P <0.05 or P <0.01), while the combined treatment group than in the treatment group alone is more obvious. Conclusions 1. Ifenprodil tartrate and ginsenoside-Rd can reduce neuronal apoptosis, reduce infarct volume and improve neurological function missing, has cerebral protection. 2 ifenprodil tartrate and ginsenoside-Rd can be reduced with the endo G NR2B positive expression, resulting in different segments of the blocking nerve cell necrosis and apoptosis. 3 ifenprodil tartrate and ginsenoside-Rd in combination can create synergies and significantly reduce infarct volume of brain injury play an important protective role.
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