芍药总甙对L-甲状腺素所致大鼠心肌肥厚的消退作用

Regressive Effect of TGP on L-thyroxine-induced Cardiac Hypertrophy in Rats

目的:考察芍药总甙对L-甲状腺素所致大鼠心肌肥厚的消退作用。方法:将大鼠随机分成4组,除了正常组,其余各组大鼠连续10天腹腔注射L-甲状腺素0.5 mg/(kg·d)造成心肌肥厚模型。第8天,给药组口服芍药总甙80 mg/(kg·d),阳性对照组口服普萘洛尔10 mg/(kg·d),模型组和正常组均以生理盐水平行处理。第11天,各组大鼠测9导心电图后处死,取标本,称全心重和左心室重,计算心脏指数,用试剂盒(比色法)测定各组心、脑、肾线粒体ATP酶活性及丙二醛含量,记录胸主动脉由去甲肾上腺素引起的收缩反应。结果:与模型组相比,芍药总甙组大鼠心脏重量参数和左心室重量参数分别下降了10.2％和12.5％(P<0.05),心肌QT离散度的增加明显减少(-13.6％,P<0.05),心脏线粒体Na+/K+-ATP酶和Ca2+/Mg2+-ATP酶活性及丙二醛含量明显下降,但其胸主动脉收缩反应无明显影响。结论:芍药总甙对L-甲状腺素所致大鼠心肌肥厚有消退作用,其作用由抑制过度活性的钠钾泵及钙泵所介导。

Objective: To investigate the regressive effect of total glucosides of Paeonia Lactiflora (TGP) on cardiac hypertrophy induced by L-thyroxine(L-Thy) in rats. Methods: The rats were randomly divided into 4 groups. Except the normal group, the cardiac hypertrophy models of rats were induced by continuous administration of L-Thy 0.5 mg/(kg·d), ip, for 10 d in other 3 groups. On d 8, TGP 80 mg/(kg·d) (in TGP group) , propranolol (in Pro group) 10 mg/(kg·d), and normal saline (in model group or normal group) were respectively administered orally. On d 11, after 9 leads of ECGs were recorded, the rats in each group were sacrificed, and their hearts were taken out and weighted. The cardiac indexes were calculated, the ATPase' s activities and MDA' s contents in their brains, hearts, and kidney mitochondria were assayed by colorimetric analysis using kits and the contraction response of rat aorta to norepinephrine was recorded. Results: Compared with model group, TGP significantly reduced HW/BW and LVW/BW by 10.2% and 12.5% (P < 0.05) , lessened QT interval dispersion ( - 13.6% , P < 0.05) , and lowered the activities of Na+ ,K+-ATPase and Ca2+ ,Mg2+-ATPase and MDA contents in brain, heart and kidney mitochondria, but it had no significant effect on the change of contraction response of thoracic aorta of rats. Conclusion: TGP has regressive effect on cardiac hypertrophy induced by L-Thy, and the effect is mediated by suppression on the over-activity of Na+ /K+ ATPase and Ca2+ /Mg2+ -ATPase.