ABSTRACT
Objective To study the effect and mechanism of endoplamic reticulum stress on the auditory cortex injury after focal cerebral ischemia-reperfusion injury in rats.Methods 30 healthy male adult SD rats were chosen and randomly divided into 2 groups,ischemia-reperfusion(I/R) group and sham operated control,with each group 15 rats.The rats in I/R group were operated for suture-occluded method to establish middle cerebral artery occlusionmodel(MCAO),with ischemia for 60 mins followed by reperfusion for 24 h.And the control group was only to be isolated cervical vessels,with no thread embolism inserted.The auditory brainstem response (ABR) was tested before operation and at 24 h post-operation respectively.The neurological deficits,ratio of infarct volume were evaluated.The pathological changes were observed by HE.Neurocyte apoptosis were observed by Tunel,and the AI were determined.The expression of GRP78,Caspase-12 were detected by immunohistochemistry and Western blotting.Results Compared with the sham group,the neurological function scores,the infarct volume of brain of I/R group increased significantly.The threshold of ABR elevated significantly and AI rised in I/R group.HE staining showed that the neurons in the sham group were arranged in order,the shape was normal,but in the I/R group the normal structure disappeared,the nuclei were condensed.The expression of GRP78,Caspase-12 protein were significantly up-regulated.All of the differences above have statistical significance(P＜0.05).Conclusion The mechanism of hearing loss after focal cerebral ischemia-reperfusion injury in rats is perhaps related to endoplamic reticulum stress,and GRP78,Caspase-12 participate in the process of neuron apoptosis on auditory cortex caused by ERS.
ABSTRACT
Objective To study the mechanism of endoplamic reticulum stress(ERS)pretreatment induced by 2-DG on the auditory cortex injury after focal cerebral ischemia-reperfusion injury in rats. Methods The SD rats were randomly divided into 3 groups,sham group,I/R group,and ERS pretreatment group. Tread occlusion was used to prepare the model of MCAO in the mice for 60 min followed by reperfusion for 24 h. Neurological assessment was exercised and brain infarction volume was evaluated. The auditory brainstem response was tested. The pathological changes were observed by HE staining. Neurocyte apoptosis was observed by Tunel ,and the apop-tosis index(AI)was determined. Expression of GRP78 and Caspase-12 were detected by immunohistochemistry. Results Compared with the sham group,the neurological scores,ratio of infarct volume and the hearing thresh-olds in I/R group increased significantly. HE staining showed the normal structure disappeared ,and apoptotic index increased significantly. Expression of GRP78 and Caspase-12 protein significantly up-regulated. Compared with I/R group,the indicators above showed improvement to some degrees. Conclusions The ERS pretreatment can alleviate the ischemia-reperfusion injury and neuron apoptosis in auditory cortex ,and reduce the possibility of hearing loss.