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目的 探讨二氢吡啶类钙拮抗剂 2 ,6 -二甲基 - 4- (3-硝基苯基 ) - 1. 4-二氢 - 3,5 -吡啶二羧 - 3-甲酯 - 5 -正戊酯(MN92 0 2 )在 L-甲状腺素 (L- thyroxine,L- Thy)引起大鼠心肌肥厚时对心脏指数 ,心肌超微结构及心肌组织超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶 (GSH- PX)活性和丙二醛(MDA)含量的影响 .方法 连续 12 d ip L- Thy0 .5 mg·kg- 1 · d- 1 复制大鼠心肌肥厚模型 ,实验组 ip MN92 0 2 0 .4mg· kg- 1· d- 1 ,2 mg·kg- 1· d- 1 ,10 mg· kg- 1· d- 1 ,阳性对照组 ip卡托普利 2 5 mg· kg- 1 · d- 1 ,模型组、对照组给予等量溶剂 ,于给药后的第 13日处死大鼠 ,检测心脏指数 ,电镜观察心肌组织的超微结构变化 ,化学比色法测定心肌匀浆中 SOD、GSH- PX活性和 MDA含量 .结果 在注射 L- Thy12 d后 ,与对照组相比 ,MN92 0 2能明显降低心脏指数 ,减轻心肌组织超微结构的病理改变 ,显著提高大鼠心肌中 SOD和 GSH- PX活性 ,并减少 MDA的生成 ,尤以中、高剂量为佳 (P<0 .0 5 ,P<0 .0 1) .结论 MN92 0 2能抑制 L - Thy所引起的心肌肥厚 ,对心肌组织具有保护作用 ,该作用与阻止 Ca2 +内流 ,防止钙超载 ,提高氧自由基清除活性 ,抑制脂质过氧化反应有关
Objective To investigate the effects of dihydropyridine calcium antagonist 2, 6 - dimethyl - 4- (3 - nitrophenyl) -1,4-dihydro-3,5-pyridinedicarboxylate- Myocardial index, myocardial ultrastructure and the activity of superoxide dismutase (SOD), glutathione (GSH) in the myocardium of n-amyl glutamate (MN92 0 2) induced cardiac hypertrophy induced by L-thyroxine Glutathione peroxidase (GSH-PX) activity and malondialdehyde (MDA) content.Methods Rat model of cardiac hypertrophy was induced by ip L- Thy0.5 mg · kg-1 · d- Group ip MN92 0 2 0 .4 mg · kg -1 · d -1, 2 mg · kg -1 · d -1, 10 mg · kg -1 · d -1, positive control group Captopril 25 mg · Kg -1 · d -1. The rats in the model group and the control group were given the same amount of solvent. The rats were sacrificed on the thirteenth day after administration. The cardiac index was measured. The ultrastructure changes of myocardium were observed by electron microscopy. SOD, GSH-PX activity and MDA content in myocardial homogenate.Results After treated with L-Thy for 12 days, compared with the control group, MN92 0 2 could obviously reduce the cardiac index and alleviate the pathological changes of myocardial ultrastructure, SOD and GSH- PX in rat myocardium (P <0.05, P <0.01) .Conclusion MN92 0 2 can inhibit the cardiac hypertrophy induced by L - Thy and inhibit the production of MDA Has a protective effect, the role and prevent Ca2 + influx, prevent calcium overload, increase oxygen free radical scavenging activity, inhibition of lipid peroxidation