摘要
目的:研究线粒体ATP敏感性钾通道(mitoKATP)参与血红素氧化酶1(HO-1)对抗心肌缺血-复灌损伤。方法:SD大鼠腹腔注射HO-1的诱导剂hemin(50mg/kg)、抑制剂ZnPP(25μg/kg)和mitoKATP通道阻断剂5-HD,24h后取离体心脏给予30min缺血和120min复灌。检测心室收缩功能、LDH、CK和心肌梗死面积。结果:①hemin诱导HO-1活性增加可改善缺血-复灌心脏的收缩功能,缩小心肌梗死面积,而ZnPP可抑制其作用。②在腹腔注射hemin前给予mitoKATP通道阻断剂5-HD(5mg/kg),与Hemin+IS组相比,心脏的收缩功能明显下降,心肌梗死面积增大,LDH和CK释放增加。而在hemin预处理后24h与30min缺血前给予5-HD灌流(100μmol/L)同样可阻断hemin诱导的心肌保护作用。结论:hemin可诱导心肌HO-1增加保护心肌缺血-复灌性损伤,而mitoKATP通道在hemin诱导的心肌保护作用中扮演了启动因子和终末效应器双重角色。
Objective：To and evaluate the effects of chromosome ATP-sensitive explore protective potassium channel participating in the activation of heme oxygenasse 1 （HO-1） against the injury of ischemia-reperfusion in the heart. Methods： HO-1 inducer heroin （50 mg/kg）, inhibitor ZnPP （25 μ g/kg） and the blocker of mitoKATP channel 5-HD were injected intraperitoneally. The isolated heart was subjected to 30 min regional ischoaia and 120 min of reperfusion. The constrictive function of the ventricles, LDH, CK and the infracted area were measured. Results： ①The increasing of the activation of HO-1 induced by hemin could improve the constrictive function of the ischemia-reperfused heart and shortened the infracted area, but ZnPP could inhibite its function; ②Compared with Heroin ＋ IS, mitoKATP blocker 5-HD （5 mg/kg） given before intraperitoneal injection of heroin could obviously decline the cardiac constrictive function, increase the cardiac infracted area and increase the releasing of LDH and CK. After pretreatment of heroin for 24 hrs, the cardiac protection induced by heroin could he similarly blocked when 5-HD was given before 30 min of ischemia. Conclusion： Hemin can protect against ischemi-reperfusion injury in the heart through enhancing of HO-1 activity, the mitoKATP channel serves as both a trigger and an effector in the protection of the heart induced by heroin.
出处
《温州医学院学报》
CAS
2006年第6期516-519,共4页
Journal of Wenzhou Medical College
基金
浙江省教育厅科研基金资助项目(20041095)
温州市科技局科研基金资助项目(Y2003A099)
