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目的:研究KATP通道开放剂尼可地尔(nicorandil,Nic)对甲状腺素诱发的大鼠心肌肥厚的作用。方法:采用大鼠连续10 d,ip,左旋甲状腺素(L-thyroxine,L-thy)造心肌肥厚模型,造模第3天开始Nic灌胃给药,共8 d。观察Nic对大鼠心重指数、组织形态学,心肌线粒体中超氧化物歧化酶(SOD)、丙二醛(MDA)含量及Na+-K+-ATP酶、Ca2+-ATP酶活力的影响;用免疫组化方法测定Nic对心肌Fas,Bcl-2蛋白表达的影响。结果:与模型组相比,Nic显著降低大鼠的心重指数及改善病理改变,提高心肌线粒体中SOD活性,减少MDA含量,并显著增加Na+-K+-ATP酶、Ca2+-ATP酶活力;Nic明显抑制肥厚心肌Fas的表达,促进Bel-2的表达。KATP通道的阻滞剂格列苯脲可减弱Nic的上述作用。结论:Nic能显著抑制L-Thy诱发的大鼠心肌肥厚,对肥厚心肌具有明显的保护作用,这可能与Nic通过开放KATP通道从而抑制心肌细胞线粒体脂质过氧化,显著改善能量供应以及减少心肌细胞凋亡等有关。
Objective: To investigate the effect of Nicorandil (KATP) channel opener on thyroxin-induced cardiac hypertrophy in rats. Methods: Cardiac hypertrophy was induced by L-thyroxine (L-thyroxine) for 10 d in rats. Nicardine administration was started on day 3 after modeling for 8 d. The effects of Nic on cardiac index, histomorphology, the content of myocardial SOD and MDA and the activities of Na + -K + -ATPase and Ca2 + -ATPase in rats were observed by immunohistochemistry Methods The effect of Nic on the expression of Fas and Bcl-2 in myocardium was determined. Results: Compared with the model group, Nic significantly reduced the cardiac index and the pathological changes of rats, increased the activity of SOD in myocardial mitochondria, decreased the content of MDA and significantly increased the activities of Na + -K + -ATPase and Ca2 + -ATPase. Nic Inhibit the expression of Fas in hypertrophic myocardium and promote the expression of Bel-2. Glibenclamide, a blocker of the KATP channel, attenuated the above effects of Nic. CONCLUSION: Nic can significantly inhibit L-Thy-induced rat cardiac hypertrophy and have a significant protective effect on hypertrophic myocardium. This may be related to the fact that Nic inhibits myocardial mitochondrial lipid peroxidation by opening KATP channels, significantly improving energy supply and decreasing myocardial Apoptosis and other related.