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目的研究葛根复方对重症肌无力大鼠心肌线粒体ATPase活性的影响,探讨重症肌无力在心肌中的发病机制。方法将80只lewis大鼠随机分为空白组和造模组,采用鼠源性AchR-α亚基97-116肽段免疫大鼠制造肌无力模型,选取造模成功的大鼠,分为模型组、强的松组及中药组,分别给予阳性对照组(强的松)和中药组(葛根复方)连续灌胃,治疗4 W后停药,检测大鼠心肌线粒体ATPase活性的变化。结果重症肌无力大鼠心肌线粒体ATPase活性明显降低,造模成功的大鼠Na+-K+-ATPase,Mg2+-ATPase,Ca2+-ATPase,Mg2+-Ca2+-ATPase活性明显低于正常组大鼠(P<0.01);经过治疗后的大鼠ATPase活性都有恢复,与模型组比较,其活性都明显升高(p<0.05);与强的松比较,中药组治疗效果更加明显(p<0.05)。结论重症肌无力可累及到心肌,葛根复方可通过促进线粒体ATPase活性的恢复治疗重症肌无力心肌病变。
Objective To study the effect of kudzu compound on myocardial mitochondrial ATPase activity in rats with myasthenia gravis and to explore the pathogenesis of myasthenia gravis in myocardium. Methods Eighty lewis rats were randomly divided into blank group and model group. Rat models of myasthenia gravis were established by immunization with murine AchR-α subunit 97-116 peptide. The model rats were selected and divided into model The rats in the control group (prednisone) and the traditional Chinese medicine group (Pueraria compound) were given gavage continuously for 4 weeks. The changes of mitochondrial ATPase activity in the myocardium of rats were observed. Results Myocardial mitochondrial ATPase activity was significantly decreased in rats with myasthenia gravis. The activities of Na + -K + -ATPase, Mg2 + -ATPase, Ca2 + -ATPase, Mg2 + -Ca2 + -ATPase in rats with successful model were significantly lower than those in normal rats (P <0.01) ). After treatment, the ATPase activity of rats recovered. Compared with the model group, the activity of ATPase was significantly increased (p <0.05). Compared with prednisone, the treatment effect of TCM group was more obvious (p <0.05). Conclusions Myasthenia gravis can affect the myocardium. Pueraria compound can treat myocardial myasthenia gravis by promoting the recovery of mitochondrial ATPase activity.