心肌线粒体ATP敏感性钾通道开放保护线粒体结构和功能

Effects of mitochondrial ATP-sensitive potassium channel opener on the structures and functions of the mitochondria

目的 评价线粒体ATP敏感性钾通道 (mitoKATP)开放剂二氮嗪对缺氧心肌线粒体结构和功能的影响。方法 异丙肾上腺素 (ISO)皮下注射诱发大鼠心肌缺氧损伤 ,观察二氮嗪对线粒体呼吸控制比 (RCR)、膜流动性、磷脂酶A2 和磷脂含量的影响。结果 ISO皮下注射诱发大鼠心肌缺氧损伤后 ,与对照组比较线粒体RCR降低了 2 0 8% (P <0 0 1) ,膜流动性降低了 9 1% (P <0 0 5 ) ,磷脂酶A2 活性增加了14 4 5 % (P <0 0 1) ,磷脂含量下降了 37 5 % (P <0 0 5 ) ,二氮嗪预防性给药后可改善RCR、膜流动性和磷脂含量。

AIM To evaluate the effects of diazoxide on the structures and functions of the mitochondria after hypoxia injury. METHODS A myocardial hypoxia injury model on rat is established by subcutaneous injection of isoproterenol (ISO) 5 mg·kg -1. The degree of oxidative phosphorylation, membrane lipid fluidity (LFU), phospholipidase A 2 activity, and phosphlipid content of mitochondria were observed after hypoxia injury. RESULTS Compared with the controls, the levels of RCR, LFU and phosphlipid content were decreased 20.8% (P<0.01), 9.1% and 37.5% (P<0.05), respectively. PLA 2 were increased by 144.5%(P<0.01). Administration of diazoxide increased RCR, LFU and phosphlipid content. CONCLUSION These results suggest that diazoxide has a protective effect on ISO-induced myocardial injury in rats.