Purpose: Cerebral ischemic stroke is one of complicated diseases in the nervous system.The aim of the current study was to analyze the effects of neuregulin1β(NRG1β)on brain tissues in a rat model of middle cerebral artery occlusion/reperfusion(MCAO/R)through inhibiting the phosphorylation of hematopoietic progenitor kinase 1(HPK1).Methods: Seventy(70 cases)healthy adult male Wistar rats were randomly divided into the sham operation group,model group and NRG1β treatment group.Laser Doppler flowmetry(LDF)was used to make records of the regional cerebral blood flow(r CBF).Rats with a post-reperfusion r CBF decline of > 30%,and a post-reperfusion r CBF recovered of 80%,were considered to be successful MCAO models.After 24 h of MCAO/R(referring to Longa’s method),neurobehavioral function was measured by modified neurological severity score(m NSS)test;brain water content was measured by dry-wet weighing method;the brain cells morphology of brain tissues was observed by hematoxylin-eosin(H&E)staining;the neurons pathological morphology was observed by Nissl staining;the apoptotic cells were counted by in situ cell death detection kit(TUNEL);the integrity of the blood brain barrier(BBB)was observed by Evans Blue(EB)staining;the expression of HPK1 was determined by immunohistochemical assay and Western bloting.Results: Compared with the sham operation group,m NSS scores were significantly increased,the water content in the brain has increased,pathology of nerve cells was obvious,number of apoptotic cells was increased,the integrity of the BBB was damaged,and the protein level of phospho-HPK1 was decreased in the model group(P<0.05).After treatment with NRG1β,the neurological function was significantly recovered,the water content in the brain has declined,the abnormal morphological structure of brain cells was ameliorated,the deformation of nerve cells was reduced,the integrity of the BBB was restored,and the protein level of phospho-HPK1 was decreased compared with the model group(P<0.05).Conclusion: NRG1β exerts a neuroprotective effect through down-regulating the expression of phospho-HPK1 in MCAO/R rats. |