Effect of hydrogen gas on endoplasmic reticulum stress and neural cell apoptosis in rats with cerebral ischemia-reperfusion injury / 重庆医学

ABSTRACT

Objective To investigate the effects of inhaling high concentration of hydrogen gas on the expressions of endoplasmic reticulum stress(ERS) related protein glucose regulated protein 78 (GRP78),Caspase-12 and the neural cell apoptosis and related proteins Bcl-2 and Bax in the rats with focal cerebral ischemia reperfusion(I/R) injury.Methods Seventy-two healthy SPF male Sprague-Dawley rats were selected and then randomly divided into the control group(Ⅰwithout any treatment),sham operation group (Ⅱ),cerebral IRI group (Ⅲ) and hydrogen gas treatment group (Ⅳ),18 cases in each group.Focal cerebral ischemia reperfusion injury (IRI) model was induced by using the suture-occluded method.The neurological deficits score (NDS) was assessed at 24 h after cerebral reperfusion in four groups.The cerebral infarction severity and size were detected by TTC staining and neuronal apoptosis of brain cortex were tested by TUNEL technique.The apoptosis index (AI) was calculated.Then the expressions of GRP78,Caspase-12,Bcl-2 and Bax were assessed by Western blot and immunohistochemistry.Results As compared with the group Ⅰ and Ⅱ,NDS score,cerebral infarction size,AI and the expressions of GRP78,Caspase-12 and Bax in cerebral cortex in the group Ⅲl and Ⅳ were significantly increased,while the expression of Bcl-2 in cerebral cortex was markedly decreased(P＜0.05);compared with the group Ⅲ,NDS score,brain infarction size,AI and the expression of Caspase-12 and Bax in cerebral cortex in the group Ⅳ were markedly decreased,while the expressions of GRP78 and Bcl-2 were dramatically increased (P＜0.05).Conclusion Inhaling high concentration of hydrogen gas has a certain protective effect on cerebral IRI in rats through increasing endoplasmic reticulum GRP78 protein expression after IRI and inhibiting Caspase-12 activation,thus inhibiting ERS and promoting the repair function of endoplasmic reticulum.