The Expression Of ERK In Focal Cerebral Ischemic In Rat And The Protection Of Naoxintong

Objective: To determine the role of extracellular signal-regulated kinase (ERK) during focal cerebral ischemia /reperfusion in rat.Methods: Male adult Wistar rats were established models of right middle cerebral artery occlusion (MCAO) with introducing a nylon suture to the right internal carotid artery.The rats were randomly devided into 2 groups: the sham operation group and the ischemia-reperfusion group(I/R group) .At different time points after I/R, the animals were designated as subgroups 3h,6h,24h,48h and 72h.The neurological deficit grades and the volume of the cerebral infarction were estimated by Zea Longa's method and 2%TTC staining .The histopathologic changes were observed by the HE staining method. The apoptosis neurons were detected in CA1 area of hippocampus by TUNEL method. ERK phosphorylation was detected by immunohistochemistry.Results: 1) The neurological deficit scores is 0 in the sham-operated group, but ranged from 2 to3 during earlier periodand (3~6h) after reperfusion . At 48h after reperfusion it obviously lessen ,and At 72h the most rats had no obviously neurological deficit. 2) The sham-operated group had no cerebral infarct sizes .The rats had their largest cerebral infarct sizes at 24h after reperfusion.3) After MCAO, the normall neurons in CA1 areas decreased. 4) A lot of apoptosis cells were observed and peaked at 48h. ERK activity increased after 3h of MCAO and peaked at 6h.Conlusion: This study demonstrates ERK plays an important role in focal cerebral ischemia.Cerebral ischemia -erperfusion may be result in the activity of ERK up-regulation,and participate the process of neurons apoptosis.Part twoThe Effect of Naoxintong on Injury after Cerebral Ischemia-Reperfusion in RatsObjective.- The purpose of this study was to evaluate l)the changes of neurologic impairment and infarct cerebral volume. 2)study the activation of extracellular signal regulated kinase(ERK) after focal cerebral ischemia-reperfusion in rats and effect of Naoxintong on it.Methods: Male adult wistar rats were randomly devided into 3 groups, the sham-operated group > the Cerebral ischemia-reperfusion and the Naoxintong group. The model of middle cerebral artery occlusion (MCAO) was established by introducing a nylon suture to the right internal carotid artery method,and befor the ischemic phase,to rats in the sham-operated group and the control group 4mL of normal saline was intragastric administration,and to rats in the Naoxintong group,0.18g/kg of Naoxintong dissolved in 4mL of normal was intragastric administration for 6 days.The rats were decapitated at 3hrs,6hrs,24hrs,48hrs ,72hrs after reperfusion.6 rats of every group at each time point. The neurological deficit grades and the volume of the cerebral infarction were estimated by 2%TTC staining and Zea Longa' s method and HE staining;ERK phosphorylation was detected by immunohistochemistry.Results: 1) there are not significant difference existed on the neurological deficit scores between the N.S and Naoxintong-treated groups.2) The sham-operated group had no cerebral infarct sizes;The rats had their largest cerebral infarct sizes at 24h after reperfusion;Naoxintong-treated group obviously cut down cerebral infarct sizes.3)The cerebral ischemia induced ERK activation reached the peak at 6hrs andmaintained to 72hrs after reperfusion.As compared with the control group,the ERK activation in the Naoxintong group was significantly enhanced with increased positive immune reacted cells. 4)As compared with the control group, the apoptosis neurons in the Naoxintong group was significantly decreased.Contusion: Naoxintong protect impaired neurone in cerebral ischemia-reperfusion injury.