丁苯酞减轻缺血性脑卒中大鼠脑缺血再灌注损伤的机制OA

Aim To investigate the neuroprotective mechanism of butylphthalide in cerebral ischemia-reperfusion injury(CIRI)in rats with ischemic cerebral stroke(ICS).Methods Totally 24 healthy male SD rats were randomly divided into sham operation group,model group,and butylphthalide group.The neurological deficit scores of each group of rats were measured,and the cerebral infarction volume and cerebral edema rate were evaluated.HE staining was used to observe pathological changes in brain tis-sue;ELISA method was used to measure the levels of superoxide dismutase(SOD),malondialdehyde(MDA),interleukin-6(IL-6),IL-1 β,and tumor necrosis factor-α(TNF-α)in brain tissue;Western blotting was used to detect the protein expression levels of JAK2,phosphorylated(p)-JAK2,signal transducer and activator of transcription-3(STAT3),p-STAT3,vascular endothelial growth factor(VEGF),and erythropoietin(EPO).Results Compared with the sham surgery group,the model group showed an in-crease in neurological deficit score,the percentage of cerebral infarction volume and cerebral edema rate,MDA,IL-6,IL-1 β,TNF-α levels,as well as p-JAK2/JAK2,p-STAT3/STAT3,VEGF,and EPO protein expression levels(P<0.05),while the SOD level in brain tissue were decreased(P<0.05).Compared with the model group,the butylphthalide group reversed the changes of the above indicators(P<0.05).The sham surgery group had intact brain tissue structure and normal cell morphology;The brain tissue struc-ture of the model group was damaged,with obvious degeneration and necrosis,shrinking and deepening of neuronal nuclei,and disor-dered cell arrangement;The morphology of brain tissue in the butylphthalide group was significantly improved compared to the model group,with relatively intact neural cell structure and reduced degree of degeneration and necrosis.Conclusion Dibenzophenone alleviates CIRI in ICS rats by regulating the JAK2/STAT3 signaling pathway,and its mechanism may be related to oxidative stress inhi-bition,inflammatory response reduction,and angiogenesis regulation.