论文标题:温阳益心安神法防治心房颤动的机理研究
Study on the Mechanism of the Rule of Strengthening Yang Invigorating Heart and Tranquilizing Preventing and Treating Atrial Fibrillation
论文作者 江畅
论文导师 曹洪欣,论文学位 博士,论文专业 中医基础理论
论文单位 黑龙江中医药大学,点击次数 610,论文页数 94页File Size16482k
2005-04-01论文网 http://www.lw23.com/lunwen_362012/ 心房颤动;温阳益心安神法;心房结构重构;心房电重构;血栓前状态;实验研究
Atrial fibrillation;The rule of strengthening yang and invigorating-heart;and tranquilizing;Atrial electrical remodeling;Atrial structural remodeling;prothrom botic state;Experience research
温阳益心安神法是导师曹洪欣教授基于多年大量临床实践总结出来的防治AF的有效法则。本文利用RT-PCR,免疫组化,光镜,电镜等技术进行了检测心房重构的相关调控因素的研究:揭示LTCC、Cox40、Cox43和ERK_2及PTS在AF发病中的作用及相互关系。观察了温阳益心安神法对其干预作用,从分子水平揭示了该法防治AF的作用机制。研究结果显示: 1、温阳益心安神法对Ach-CaCl_2诱导的AF小鼠AI增加有明显的降低作用,缩短AF持续时间,证明该法能够抑制心肌细胞肥大,延缓心房重构。 2、实验性AF小鼠血流动力学异常改变,温阳益心安神法通过提高LVSP水平,降低LVEDP水平,增强心肌舒缩功能,提高CO,降低心率,从而对改善血流动力学具有明显效果。 3、Ach-CaCl_2诱导AF小鼠心肌细胞凋亡,温阳益心安神法能够明显抑制心肌细胞凋亡,保护心脏超微结构,在病理形态学方面优势显著,降低AF小鼠死亡率。可能与拮抗ERK_2的激活,上调Cox40、Cox43水平有关。 4、实验性AF小鼠PTS异常表达,温阳益心安神法能够抑制PTS的发生,明显降低血浆中PTS分子标志物GMP-140,DD,TAT的含量,阻止严重血栓栓塞并发症的发生。 5、Ach-CaCl_2诱导AF小鼠心肌细胞Cox40、Cox43mRNA与蛋白表达下调,上调心肌细胞Cox40、Cox43mRNA与蛋白表达的水平,可能是温阳益心安神法抑制心房结构重构的作用机制。 6、Ach-CaCl_2诱导AF小鼠心肌细胞LTCCmRNA表达的下降,明显上调LTCCmRNA表达的水平,可能是温阳益心安神法抑制细胞内Ca~(2+)超载,阻止AER发生的主要作用机制。 7、Ach-CaCl_2诱导AF小鼠心肌细胞ERK_2mRNA与蛋白表达增加,激活ERK_2的同时抑制心肌细胞Cox40,Cox43mRNA与蛋白表达,可能是温阳益心安神法阻止心房间质纤维化的进
Strengthening yang and invigorating-heart and tranquilizing is effective recipe to cure atrial fibrillation which professor CaoHongXin summarizes from long-term clinical practice.Utilizing the techniques, such as RT-PCR, immunohistochemistry, optical microscope, electron microscope, the paper investigates the effect of the regulating factors of atrial electrical remodeling(AER) and atrial structural remodeling (ASR) Cox40、 Cox43、 LTCC、 ERK_2and prothrom botic state on atrial fibrillation (AF), meanwhile, observes the intervening effect of the rule of strengthening yang and invigorating-heart and tranquilizing.This paper studies the mechanism of AF and the rule on molecular level.The results show that:1、 The heart weight index and AF duration increases in the AF mouses, the rule suppresses the myocardial hypertrophy, delay atrial muscular remodeling.2、 The hemodynamics is abnormal in experimental mouses with AF, the rule improves the cardiac function through enhancing the level of LVSP and lowering the level of LVEDP and increasing cardiac output and lowering the heart rates, and improving the cardiac systole and diastole effectively.3、 Ach-CaCl2 induces myocardial apoptosis.The rule inhibits apoptosis and myocardial fibrosis ,protecting the ultrastructure and decrease the motality. through antagonizing the abnormal activation of ERK_2, up-regulating the expression of Cox40、 Cox43 mRNA and protein.4、 The prothrom botic state is abnormal expressed in AF mouses, the rule suppresses the prothrom botic state, decreases the plasma concentration of GMP140, DD, TAT significantly.5、 Ach-CaCl_2 induces the decreased expression of Cox40、 Cox43 mRNA and protein in AF mouses.The rule up-regulates the expression of Cox40、 Cox43 mRNA and protein, which maybe the therapeutic mechanism of inhibiting ASR.
|
