目的 探讨瞬态受体电位香草酸 1（TRPV1）对小鼠脑缺血再灌注后血脑屏障损伤及焦虑样行为的作用及机制。方法 线栓法构建大脑中动脉栓塞（MCAO）模型。侧脑室注射Capsazepine（CPZ，7.5 μg/ 3 μL）。HE 染色检测杏仁核区病理变化；免疫荧光染色检测杏仁核区血管损伤情况；免疫印迹技术检测 p⁃JNK、p⁃p38 MAPK的水平；高架十字迷宫检测焦虑样行为。结果 （1）与I/R组比较，I/R+CPZ组在高架十字 迷宫开臂的移动距离和停留时间显著升高（P < 0.001）。（2）与I/R组比较，I/R+CPZ组HE染色细胞核固缩减 少，水肿减少。（3）与 I/R 组比较，I/R+CPZ 组 Claudin5 表达增多。（4）与 I/R 组比较，I/R+CPZ 组 p⁃JNK、p⁃p38 MAPK水平明显降低（P < 0.05）。结论 抑制TRPV1能够通过降低p⁃JNK、p⁃p38 MAPK水平减轻小鼠脑缺血 后血脑屏障损伤及焦虑样行为。

Objective To explore the effect of TRPV1 on blood⁃brain barrier injury and anxiety⁃like behaviors after cerebral ischemia⁃reperfusion in mice and its and mechanism. Methods A model of middle cerebral artery embolism（MCAO）was constructed by use of thread embolization. Capsazepine（CPZ）of 7.5 μg/3 uL was injected into the lateral ventricle. HE staining was used to detect pathological changes in amygdala；Immunofluores⁃ cence staining was applied to detect vascular damage in amygdala；Western blot was used to detect levels of p⁃JNK and p ⁃ p38 MAPK；High plus maze was used to detect anxiety ⁃like behaviors. Results As compared with I/R group，the moving distance and length of stay in the open arms of high plus maze in I/R+CPZ group increased significantly（P < 0.001）. HE staining showed that nucleus pyknosis and edema，as compared with I/R group， were reduced in I/R + CPZ group. As compared with I/R group，Claudin5 expression was increased in I/R + CPZ group，whereas levels of p⁃JNK and p⁃p38 MAPK were significantly reduced（P < 0.05）. Conclusions Inhibition of TRPV1 can alleviate damage in blood⁃brain barrier and anxiety⁃like behaviors after cerebral ischemia in mice by reducing levels of p⁃JNK and p⁃p38 MAPK.