Auditory Center injury after Focal Cerebral Ischemia-reperfusion Injury in RATS

LV Zhe; ZHANG Ying; ZHANG Yubo; SHI Meijuan; MENG Qing; LU Hong

doi:10.3969/j.issn.1672-2922.2017.02.016

Abstract：Objective To investigate the mechanism of auditory center injury and hearing loss after focal cerebral ischemia-reperfusion injury in rats. Methods Sixty healthy male adult SD rats were randomly divided into an isch-emia-reperfusion (I/R) group and a sham operation group (n=30 in each group). For rats in the I/R group, the middle ce-rebral artery occlusion (MCAO) model was established by suturing, with ischemia for 60 mins followed by reperfusion for 24 hrs;while for those in the control group, only cervical vessels isolation was performed with no thread embolism inserted. The auditory brainstem response (ABR) was tested before and at 24 hrs after operation, respectively. At 24 hrs post-operation, neurological function, changes of water content in the brain (using dry-wet weight method) and infarct volume (using TTC method) were measured. The integrity of blood-brain barrier (BBB) was also evaluated by viewing exudation of Evans blue, and apoptosis of neurocytes was examined by TUNEL to determine the apoptotic index (AI). Expression of MMP-9, Claudin-5, Occludin, PSD-95, CX-43 and Na+-α protein were tested by Western blotting. Re-sults Compared with the sham operation group, neurological function scores, infarct volume and water content of brain were higher with elevated ABR thresholds and AI in the I/R group. Expression of MMP-9 and CX-43 protein was signifi-cantly up-regulated, while expression of Claudin-5, Occludin, PSD-95 and Na+-αprotein was significantly down-regu-lated. Conclusions The mechanism of hearing loss after focal cerebral ischemia-reperfusion injury is perhaps related to MMPs activation, BBB damage, gap junction activation, synaptic dysfunction and destruction of ion channels.