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It has been widely accepted that autophagic cell death exacerbates the progression of cerebral ischemia/reperfusion(I/R).Our previous study revealed that overexpression of reticulon protein 1-C(RTN1-C)is involved in cerebral I/R injury.However,the underlying mechanisms have not been studied intensively.This study was designed to evaluate the effect of RTN1-C on autophagy under cerebral I/R.Using an in vitro oxygen-glucose deprivation followed by reoxygenation and a transient middle cerebral artery occlusion model in rats,we found that the expression of RTN1-C protein was significantly upregulated.We also revealed that RTN1-C knockdown suppressed over-activated autophagy both in vivo and in vitro,as indicated by decreased expressions of autophagic proteins.The number of Beclin-1/propidium iodide-positive cells was significantly less in the LV-shRTN1-C group than in the LV-shNC group.In addition,rapamycin,an activator of autophagy,aggravated cerebral I/R injury.RTN1-C knockdown reduced brain infarct volume,improved neuro-logical deficits,and attenuated cell vulnerability to cerebral I/R injury after rapamycin treatment.Taken together,our findings demonstrated that the modulation of autophagy from RTN1-C may play vital roles in cerebral I/R injury,providing a potential therapeutic treatment for ischemic brain injury.