摘要
目的建立大鼠脑缺血再灌注损伤模型,探讨应用瞬时受体电位通道香草酸亚型4(TRPV4通道)抑制剂是否能够减轻脑缺血再灌注损伤诱导的血脑屏障(blood brain barrier, BBB)开放和可能机制。方法制备大鼠局灶性脑缺血再灌注损伤模型;给予TRPV4抑制剂HC067047进行处理,Evans blue检测脑缺血再灌注后BBB通透性变化,Western bolt检测脑缺血组织中caveolin-1的表达水平。结果大鼠局灶性脑缺血再灌注后,BBB通透性和脑缺血组织中caveolin-1的表达水平明显增加,给予TRPV4抑制剂HC067047后,其BBB通透性和caveolin-1的表达水平明显减少。结论 TRPV4通道抑制减轻脑缺血再灌注诱发的BBB开放,与减少caveolin-1的表达水平相关。
Objective To establish the model of cerebral ischemic reperfusion injury in rats, and study the effect and possible mechanism of transient receptor potential vanilloid 4 channel(TRPV4) channel antagonist on blood brain barrier(BBB) opening in focal cerebral ischemic reperfusion injury of rats. Methods The model of cerebral ischemic reperfusion injury in rats were prepared, and rats were treated with TRPV4 inhibitor HC067047, the permeability of BBB was determined by Evans blue and caveolin-1 expression in cerebral ischemic tissue was detected by Western bolt. Results BBB permeability and caveolin-1 expression level of cerebral ischemic tissue were both increased obviously after cerebral ischemic reperfusion in rats, but decreased prominently after treatment of TRPV4 inhibitor HC067047. Conclusion Inhibition of TRPV4 channel can reduce BBB open induced by cerebral ischemic reperfusion, which is related to the reduced caveolin-1 expression.
作者
陆威成
董子恒
解辉
LU Wei-cheng;DONG Zi-heng;XIE Hui(Department of Neurosurgery,First Affiliated Hospital of China Medical University,Shengyang,110001;Department of Neurosurgery,Central Hospital,Changtu,Changtu 112500;Department of Histology and Embryology,Shengyang Medical College,Shengyang 110034,China)
出处
《解剖科学进展》
2019年第6期655-657,共3页
Progress of Anatomical Sciences
基金
辽宁省教育厅科学技术研究项目(L2015535)
