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目的 建立大鼠脑缺血再灌注损伤模型,探讨TRPV4通道在脑缺血再灌注损伤中的作用和可能机制.方法 制备大鼠局灶性脑缺血再灌注损伤模型;检测脑缺血再灌注后0h、6h、12h、24、48h、72h、96h、7d的血脑屏障(BBB)通透性变化;给予TRPV4抑制剂HC067047或生理盐水进行处理,检测脑缺血再灌注后6h、72h、7d的BBB通透性变化,Western bolt检测脑缺血组织中MMP-9的表达水平.结果 大鼠局灶性脑缺血再灌注后,BBB通透性明显增加,于72h达峰值.脑缺血再灌注6h,72h,7d分别给予TRPV4抑制剂HC067047后,其BBB通透性较相同时间点的生理盐水处理组明显降低;同时脑缺血再灌注6h,72h,7d分别给予HC067047后,其MMP-9的表达较相同时间点的生理盐水处理组明显减少.结论 抑制TRPV4通道可以减轻脑缺血再灌注诱发的BBB开放,其机制可能与减少MMP-9的表达相关.“,”Objective To establish the model of cerebral ischemic reperfusion injury in rats,and determine the role and possible mechanism of TRPV4 channel in cerebral ischemic reperfusion injury.Methods The model of cerebral ischemic reperfusion injury in rats were prepared,the permeability of blood brain barrier (BBB) was determined at 0h、6h、12h、24、48h、72h、96h、7d after injury.The models were treated with TRPV4 inhibitor HC067047 or saline,MMP-9 expression was determined by Western bolt at 6h、72h、7d after injury.Results After cerebral ischemic reperfusion in rats,BBB permeability was increased obviously,peaked at 72h compared with treatment of saline.TRPV4 inhibitor HC067047 downregulated BBB permeability and MMP-9 expression level prominently compared with treatment of saline.Conclusion Inhibition of TRPV4 channel reduced BBB open induced by cerebral ischemic reperfusion,which may be related to the downregulation of MMP-9 expression.