Department of Cardiology, the First Affiliated Hospital of Anhui Medical University, Hefei, China.
J Cardiovasc Med (Hagerstown). 2012 Aug;13(8):511-5. doi: 10.2459/JCM.0b013e3283542031.
To study the protective mechanism of nicorandil on myocardial ischemia-reperfusion injury.
Fifty rats were randomly divided into five groups, four of which were operated on to produce myocardial ischemia-reperfusion. Nicorandil (5 mg/kg) was administrated by intravenous injection to three of the groups. The myocardial ultrastructure was observed by electron microscope. The expression levels of the antiapoptotic protein Bcl-2 and the pro-apoptotic protein Bax were detected by immunohistochemical staining with rhodamine 123. The mitochondrial membrane potential was detected by spectrophotometry.
The activity of lactate dehydrogenase (LDH) and malondialdehyde (MDA) content was decreased and the activity of superoxide dismutase (SOD) was increased in the three nicorandil groups, compared with those in the group without nicorandil (P < 0.01, P < 0.05). The positive staining level of the expressed Bcl-2 was increased and the expressed Bax was decreased (P < 0.01) in the three nicorandil groups, compared with those in the group without nicorandil. The mitochondrial inner membrane potential was increased in the three nicorandil groups compared with that in the group without nicorandil (P < 0.05).
A suitable level of nicorandil has a protective effect on rats' myocardial ischemia-reperfusion injury, and is mainly based on the opening of the mitochondrial KATP channel and the lowing of Ca overload.
研究尼可地尔对心肌缺血再灌注损伤的保护作用。
将 50 只大鼠随机分为 5 组，其中 4 组进行心肌缺血再灌注手术。3 组静脉注射尼可地尔（5mg/kg）。用电子显微镜观察心肌超微结构。用罗丹明 123 免疫组化染色检测抗凋亡蛋白 Bcl-2 和促凋亡蛋白 Bax 的表达水平。用分光光度法检测线粒体膜电位。
与未用尼可地尔的组相比，3 个尼可地尔组的乳酸脱氢酶（LDH）活性和丙二醛（MDA）含量降低，超氧化物歧化酶（SOD）活性升高（P<0.01，P<0.05）。3 个尼可地尔组的 Bcl-2 表达阳性染色水平升高，Bax 表达降低（P<0.01）。与未用尼可地尔的组相比，3 个尼可地尔组的线粒体内膜电位升高（P<0.05）。
适量的尼可地尔对大鼠心肌缺血再灌注损伤具有保护作用，主要基于线粒体 KATP 通道的开放和 Ca 超载的降低。
