Abstract:

[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 for1h followed by24-h reperfusion. In group HPC,8% oxy?gen was inhaled for3h at12h before ischemia. No nylon suture was inserted in group S. Neurological deficits were assessed at the end of24-h reperfusion. And then rats were decapitated. The expressions of growth arrest and DNA-damage-inducible 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 GADD153protein was significantly up-regulated, in group I/R and group HPC than those in group S. The neurological deficit score and apoptotic index were significantly lower, the GADD153protein expression was significantly down- regulated, in group HPC than those in group I/R (allP<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 GADD153protein expression in cerebral cortex.

Key words: reperfusion injury, endoplasmic reticulum, stress, cerebral cortex, hypoxia preconditioning