基于VEGF/PI3K/AKT信号通路探讨贝伐珠单抗对缺血性脑卒中小鼠的影响及作用机制OA

Objective:To investigate the effect and mechanism of bevacizumab(BEV)on ischemic stroke injury.Methods:Male C57BL/6J mice were used to establish a middle cerebral artery occlusion(MCAO)model.A total of 42 C57BL/6J mice were randomly assigned into three groups:Sham group,MCAO group,and BEV group,with 14 mice in each group.The effects of BEV on MCAO mice were detected by Zea-Longa score,TTC staining,H&E staining,Nissl staining,immunohistochemis-try,and Western blot.Results:Compared to the Sham group,mice in the MCAO group exhibited increases in the Zea-Longa score and the percentage of cerebral infarct volume(P<0.01).The morphological structure of brain tissue cells on the ischemic side was disrupted,with significant neuronal injury and a reduction in Nissl body content.Additionally,there were decreases in the protein expression levels of VEGF,AKT,and PI3K,as well as Bcl-2/Bax and P-AKT/AKT protein ratios(P<0.01).Com-pared to the MCAO group,mice in the BEV group showed significant increases in the Zea-Longa score and the percentage of cere-bral infarct volume(P<0.01).The morphological structure of brain tissue cells on the ischemic side was more severely disrupted,with more pronounced neuronal injury and a significant reduction or even disappearance of Nissl bodies.The expression level of PI3K protein was decreased(P<0.05),and the expression level of VEGF protein,Bcl-2/Bax and P-AKT/AKT protein ratios were further significantly reduced(P<0.05).Conclusion:BEV aggravates the injury in mice with ischemic stroke,and its mecha-nism may be related to the VEGF/PI3K/AKT signaling pathway.