Rho/Rho激酶信号通路在缺氧性肺血管收缩中的机制  

Role of the Rho/Rho-kinase pathway in the mechanism of hypoxic pulmonary vasoconstriction

作　　者：梁迪[1] 韩思莹[1] 宋小丹[1] 梁淑俊[1] 

机构地区：[1]哈尔滨医科大学药学院,黑龙江哈尔滨150081

出　　处：《哈尔滨医科大学学报》2009年第3期226-228,共3页Journal of Harbin Medical University

摘　　要：目的探讨15-羟基二十碳四烯酸(15-HETE)致大鼠肺动脉收缩的信号转导途径,阐明15-HETE引起慢性缺氧性肺动脉收缩作用的可能机制。方法采用组织浴槽血管环方法测量15-HETE对缺氧模型组、正常组大鼠血管收缩作用,并观察加入Rho激酶抑制剂Y-27632后肺动脉环收缩强度的改变,明确Rho/Rho激酶信号转导途径在15-HETE收缩肺动脉中的作用。结果15-HETE对正常组、缺氧模型组大鼠血管环均有收缩作用,当加入Rho激酶抑制剂Y-27632可明显阻断15-HETE对缺氧大鼠肺动脉的收缩作用(P<0.05)。结论15-HETE通过Rho/Rho激酶信号转导途径收缩慢性缺氧性大鼠肺动脉。Objective To observe the signaling pathway of 15-hydroxyeicosatetraenoicacid（15-HETE） induced pulmonary artery constriction of rats,and clarify the possible mechanism of 15-HETE induced hypoxic pulmonary vasoconstriction. Methods Pulmonary arterial rings were used to assess the role of 15- HETE in pulmonary artery tension from hypoxic and normoxic rats,furthermore,the inhibitor of Rho-kinase signaling pathway was employed to determine the role of Rho/Rho-kinase signaling pathway in 15- HETE induced pulmonary vasoconstriction. Results 15~HETE constricted the pulmonary artery rings of both hypoxic and nomorxic rats ;and Y-27632 reduced 15-HETE vasoconstriction effect significantly（P 〈 0.05）. Conclusion 15-HETE constricts the pulmonary arteries of rats in chronic hypoxia via Rho/Rho- kinase signaling pathway.

关 键 词：缺氧性肺血管收缩 15-羟基二十碳四烯酸 RHO激酶 Y-27632 肺动脉环 

分 类 号：R-332[医药卫生] R322.12