Influences Of Limb Ischemic Preconditioning On Autophagy In Rats With Cerebral Ischemia Reperfusion Injur

Objective: Acute ischemic stroke(Acute ischemic stroke,AIS)is a complex multifactorial disease.The traditional treatment is to restore the blood perfusion of ischemic area,but this method can cause ischemia reperfusion injury(IRI).In this case,the need for new measures to protect nerve exploration,limb ischemia postprocessing(LPostC)is the organ or tissue after ischemia reperfusion,immediately once or several times of transient ischemia and reperfusion of limbs,to improve the organization of ischemic tolerance.However,the mechanism of action of LPostC has not been fully understood,especially the mechanism of autophagy.Methods: 60 Wistar rats were randomly divided into sham operation group(Sham group),ischemia reperfusion group(I/R group),limb ischemic preconditioning group(LIPC group),3-methyladenine group(3-MA group),each group had 15 rats.Production of cerebral ischemia reperfusion,LIPC and 3-MA in rats,the neurological function score and infarct volume were measured after cerebral ischemia 2h reperfusion 24 h,cell morphology was observed by HE staining,Western Bloting method to detect autophagy related protein Beclin-1?Cathepsin B.Results: 1.The neurological deficit score:Sham group was sensitive and no neurological dysfunction.Compared with Sham group,I/R group,LIPC group and 3-MA group had different degrees of neurological dysfunction(P<0.05).Compared with I/R group,the symptom score of LIPC group was significantly lower(P<0.05).There was no significant difference between LIPC group and 3-MA group(P>0.05).2.Cerebral infarction volume measurement:After TTC staining,the brain tissue of the naked eye Sham group was red,no cerebral infarction.Compared with the Sham group,I/R group,LIPC group,3-MA group had different degrees of cerebral infarction(P<0.05),the infarct area was white,and the infarct area of I/R group was the largest.Compared with I/R group,LIPC group,cerebral infarction volume decreased significantly(P<0.05);compared with LIPC group,3-MA group,cerebral infarction volume decrease(P<0.05).3.Morphological observation:After HE staining,the morphology of the cells in the Sham group was normal,the cell membrane was complete,the nucleus was located in the cytoplasm,and Nissl bodies were found in the cytoplasm.Compared with Sham group,I/R group showed acute ischemic changes of cells,cytoplasm crimson staining,cell shrinkage deformation,nuclear pyknosis,Nissl body disappeared(P<0.05).Compared with I/R group,the pathological changes of brain tissue in LIPC group were significantly reduced(P<0.05).Compared with LIPC group,the 3-MA group had reduced cell damage(P<0.05).4.The expression of autophagy related protein Beclin-1and Cathepsin B after cerebral ischemia reperfusion in each group :Compared with Sham group,I/R group,Beclin-1?Cathepsin B expression of protein was significantly increased(P<0.05);compared with I/R group,LIPC group,Beclin-1 ? Cathepsin B expression of protein was significantly decreased(P<0.05);compared with LIPC group,3-MA group,Beclin-1 ? Cathepsin B decreased expression of protein(P<0.05).Conclusion:(1)I/R can activate autophagy and cause brain damage.(2)LIPC may play a protective role in IRI rats by reversing the overexpression of autophagy related protein Beclin-1 and Cathepsin B.(3)autophagy inhibitor 3-MA can enhance the brain protective effect of LIPC.