摘要
目的探讨细胞凋亡在大鼠心肌肥厚形成中的作用及L精氨酸(LArg)对这一过程的影响。方法36只大鼠随机分为对照组、模型组和给药组,制作压力超负荷性心肌肥厚模型,观察各组大鼠的动脉收缩压(SBP)和心脏指数,采用分光光度法和流式细胞术测定一氧化氮(NO)含量、超氧化物歧化酶(SOD)活性和心肌细胞凋亡率。结果与对照组相比,模型组大鼠SBP、心脏指数与心肌细胞凋亡率升高,SOD活性与NO水平下降;与模型组相比,给药组大鼠SBP、心脏指数与心肌细胞凋亡率降低,SOD活性与NO水平升高。结论细胞凋亡是压力超负荷性心肌肥厚发生过程中导致心肌细胞数量减少的重要原因;LArg可诱导NO生成增多,并通过增强SOD的活性抑制心肌细胞凋亡的发生。
Objective To investigate the role ot apoptosis played in myocardial hypertrophy and the effect of L-arginine （L-Arg） on the pathogenesis. Methods 36 rats were randomly divided into the control group, model group and L-Arg treating group. The animal model of over-loading myocardial hypertrophy was made, and systolic blood pressure （SBP）and the cardiac indexes were measured, spectrophotography and flow cytometry were used to detect the content of nitric oxide （NO）, activity of superoxide dismutase （SOD） and apoptosis rate. Results In the model group, SBP, cardiac indexes and myocardial apoptosis rate increased, the content of NO and activity of SOD decreased compared with the control group. While, in the L-Arg treating group, SBP, cardiac indexes and apoptosis rate decreased, the content of NO and the activity of SOD increased compared with the model group. Conclusion Myocardial apoptosis may play an important role in the pathogenesis of myocardial hypertrophy and cause the losing of myocardial cells. L-Arg induces the increasing production of NO and inhibits myocardial apoptosis through increasing the activity of SOD.
出处
《中国康复理论与实践》
CSCD
2005年第8期616-617,共2页
Chinese Journal of Rehabilitation Theory and Practice
关键词
心肌肥厚
一氧化氮
L-精氨酸
细胞凋亡
myocardial hypertrophy
nitric oxide
L-arginine （L-Arg）
apoptosis
