尼可地尔对心肌肥厚模型大鼠的保护作用及机制研究

目的:研究尼可地尔(Nic)对甲状腺素诱发大鼠心肌肥厚的保护作用。方法:大鼠连续10d腹腔注射甲状腺素建立心肌肥厚模型,3d后分别灌胃给予Nic低、高剂量8d,测定并观察Nic对大鼠心肌组织形态、超氧化物歧化酶(SOD)、丙二醛(MDA)含量及钙调神经磷酸酶(CaN)活性的影响;采用逆转录-聚合酶链反应法检测心肌c-fos、c-jun及TGF-β1mRNA表达;采用酶链免疫吸附法检测TGF-β1蛋白表达。结果:与模型组比较,Nic能显著改善肥厚心肌组织的病理改变,提高心肌SOD活性,降低MDA含量,并显著抑制CaN活性(P<0·01);下调心肌c-fos、c-jun及TGF-β1mRNA表达(P<0·05);降低TGF-β1蛋白的含量(P<0·01)。结论:Nic能显著抑制甲状腺素诱发的大鼠心肌肥厚,对心肌具有明显的保护作用。

Protective Effects of Nicorandil on Cardiac Hypertrophy in Rats Model and Its Mechanism

OBJECTIVE:To assess the effect of nicorandil(Nic) on cardiac hypertrophy induced by thyroxine in rats. METHODS:Cardiac hypertrophy was established by administration of L-thyroxine for 10 days,3 days after,the low and high dose of Nic were administratived by intragastric for 8 days,morphological changes of cardiac tissue, the activities of superoxide dismutase (SOD), the content of malondialdehyde (MDA) and calcineurin(CaN) were determined. Expression of c-fos,c-jun and TGF-β1 mRNA was examined by RT-PCR;TGF-β1 protein levels were also measured by ELISA. RESULTS:Nic remarkably improved morphological changes,significantly increased the activities of SOD, decreased the content of MDA and CaN(P<0.01),induce the expression of c-fos、c-jun and mRNA expression of TGF-β1(P<0.05) and decrease protein expression of TGF-β1 (P<0.01). CONCLUSIONS:Nic could prevent cardiac hypertrophy induced by L-thyroxine and protect cardiac tissue from injury.