Effects of Hypoxia Preconditioning on Endoplasmic Reticulum Stress Induced by Cerebral Ischemia-Reperfusion in Rats

SUN Chengliang; L Guoyi; ZHAO Zhibin

doi:10.3969/j.issn.0253-9896.2013.10.016

Abstract：Objective To investigate the effect of hypoxia preconditioning (HPC) on endoplasmic reticulum stress induced by cerebral ischemia-reperfusion (I/R) in rats.Methods Thirty-six male SD rats were randomly divided into three groups equally with twelve rats each:sham operation group (group S), group I/R and group HPC. The rat model of focal cere-bral I/R was produced by occluding right middle cerebral artery for 1 h followed by 24-h reperfusion. In group HPC, 8%oxy-gen was inhaled for 3 h at 12 h before ischemia. No nylon suture was inserted in group S. Neurological deficits were assessed at the end of 24-h reperfusion. And then rats were decapitated. The expressions of growth arrest and DNA-damage-induc-ible gene 153 (GADD153) protein in ischemic penumbra cerebral cortex were determined by immunohistochemical staining. The apoptotic neurons were detected by TUNEL assay, and the apoptotic index was calculated. Results The neurological deficit score and apoptotic index were significantly higher, the expression of GADD153 protein was significantly up-regulat-ed, in group I/R and group HPC than those in group S. The neurological deficit score and apoptotic index were significantly lower, the GADD153 protein expression was significantly down-regulated, in group HPC than those in group I/R (all P <0.05). Conclusion Hypoxia pretreatment can reduce the focal cerebral I/R-induced neuronal apoptosis mediated by endo-plasmic reticulum stress, which may be related with the down-regulation of GADD153 protein expression in cerebral cortex.