The protective mechanism of TRPV4 channel inhibitor on blood-brain barrier damage after traumatic brain injury in rats
10.16753/j.cnki.1008-2344.2024.02.013
- VernacularTitle:TRPV4通道抑制剂对大鼠创伤性脑损伤后血脑屏障破坏的保护机制研究
- Author:
Fanhao KONG
1
;
Hongyang ZHANG
;
Wei ZHANG
;
Mengze TANG
;
Yingqiao WANG
;
Xiang LI
;
Xiaohui DING
;
Zhihang YANG
;
Hui XIE
Author Information
1. 沈阳医学院基础医学院,辽宁 沈阳 110034
- Keywords:
TRPV4 channel;
PKC-δ signaling pathway;
traumatic brain injury;
blood-brain barrier
- From:
Journal of Shenyang Medical College
2024;26(2):175-178
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the protective mechanism of TRPV4 channel inhibitor on blood-brain barrier(BBB)damage after traumatic brain injury(TBI).Methods:The TBI rat model was established.TRPV4 channel inhibitor HC067047 or PKC-δ inhibitor Rottlerin was used to detect changes in BBB permeability,neurological function score,and the expression of microvascular endothelial tight junction proteins ZO-1 and ZO-2 in brain injury areas after TBI.Results:Compared with the Sham group,BBB permeability significantly increased,brain neurological function score significantly decreased,and the expression of ZO-1 and ZO-2 significantly decreased in TBI group(P＜0.05).Compared with the TBI group,after administration of HC067047 or Rottlerin,changes in BBB permeability,brain neurological function score,the expression of ZO-1 and ZO-2 were partially reversed(P＜0.05).Conclusions:TBI-induced BBB injury may be mediated by TRPV4 channel regulating PKC-δ signaling pathway to affect the expression of tight junction proteins ZO-1 and ZO-2.Inhibition of TRPV4 channel function or PKC-δ signal molecule can partially alleviate BBB damage induced by TBI.This study may provide new ideas for the treatment of clinical TBI.
