Marina Was Added To Switzerland For Ischemic Stroke Model Rats And The Protective Effects Of Mechanism Research

Objectives By comparing and neural function defect scale Longa5 method,TTC staining method measuring the cerebral infarction volume change,using immunohistochemical method to detect the rat cortex GFAP(Glial fibrillary acidic portein),cell apoptosis,expression of Caspase 3,discusses its for add marina GFAP of cerebral infarction rats,the influence of Caspase-3 expression level,and then discusses its for add marina(Retigabine RTG)the protective effect of ischemic cerebral apoplexy model rats and the mechanism.Methods Methods Seventy-five Sprague-Dawley rats were randomly divided into sham operation group(Sham group),model group(15rats,MCAO group)and intervention group(45rats,RTG group).The rats in the intervention group were divided into RTG 0h group,RTG 1h group and RTG 3h group,15 rats in each group according to the time of reperfusion.The rat tail vein was administered at different time points set.Dose: RTG(10mg / kg).Sham operation group and model group were given the same volume of saline.Longa5 method was used to compare neurological deficit score,TTC staining was used to measure cerebral infarct volume,and immunohistochemistry was used to detect the expression of Caspase-3 in astrocytes and GFAP.The neurological deficits of the three groups were assessed by Neurolgical Sevrity Scor.The rats were sacrificed and the brain tissue was obtained.TTC staining was used to evaluate the neurological deficits.The expression of Caspase-3 in cortical astrocytes and GFAP and the number of positive cells were observed under immunohistochemistry.The expression of Caspase-3 was observed by immunohistochemistry after cerebral ischemia.The data were analyzed by SPSS17.0statistical software.The data were analyzed by±s(mean±standard deviation).The t test was used to compare the three groups at the same time.The same group of subgroups were analyzed by one-way ANOVA?Results 1 Neurological deficit score: sham operation group neurological deficit score of 0points,that is,sham operation group without neurological deficit symptoms,model animals have shown a certain degree of neurological deficit symptoms,manifested as: the body curled up,the body balance capacity decreased,To the left side of the rotation,dumping,can not walk and so on.Compared with the model group,the neurological deficit score of the intervention group was significantly lower(P<0.05),showed a single neurological deficit symptoms,or combined with two neurological deficits,but the difference between the groups was not statistically significant.2 TTC staining: TTC images showed no infarction in the sham operation group.The brain tissue of the model group showed different degrees of infarction.There were no infarcts in the brain tissue of the sham operation group.There was no significant difference in the infarct volume between the model group and the intervention group at 0h,1h and 3h after intervention group.The volume of cerebral infarction in the intervention group was significantly lower than that in the model group(P<0.05).3 Immunohistochemical staining showed that the number of GFAP and the expression of Caspase-3 cells were observed in the sham operation group.The expression of Caspase-3 in astrocytes and GFAPwas significantly higher than that in the control group(P<0.05),but there was no significant difference between the two groups.Conclusions 1 Pretreatment can significantly reduce the neurological score of rats with cerebral infarction.2 The pretreatment of ritabine can reduce the expression of GFAPand apoptotic Caspase-3 in rat cerebral infarction,which may protect the ischemic stroke in rats.The mechanism may be that It is possible to reduce the excitability of neurons in cerebral ischemia by reducing the excitability of neurons and reduce the release of glutamate and further reduce the inflammatory reaction in the surrounding area of cerebral infarction,Inhibition of neuronal apoptosis,but time-dependent remains to be studied.