ACCFAHA和中国心力衰竭指南_看心衰治疗–—芪参益气滴丸.ppt

《芪参益气滴丸抗心肌缺血再灌注损伤与能量代谢的相关研究》 这篇文章发表于《国际心脏病学杂志》，此期刊影响因子为7.07 对照组 不使用芪参益气滴丸，进行缺血再灌注损伤的研究 试验组 使用不同剂量芪参益气滴丸，进行缺血再灌注损伤的研究，对比结果。 * 此试验部分是观察芪参益气滴丸对缺血后心肌血流的影响 心肌血流量检测 1. 检测5组在多个时间点缺血90分钟再灌注心肌血流量（MBF）状态。 2. QSYQ+缺血再灌注组MBF明显高于缺血再灌注组（无芪参益气滴丸），且剂量越高MBF增加越明显（P0.05） 。图A 3. 24小时后观察，缺血再灌注组MBF与对照组比仍明显缺少，而QSYQ组+缺血再灌注组MBF增加非常显著（P0.05） 。图C 从而说明芪参益气滴丸可以显著增加缺血后心肌血流 * 多篇研究都发现芪参益气滴丸对心肌能量代谢有改善作用，可能是芪参益气滴丸参与能量代谢的改变，对于相关mRNA有调节作用，对线粒体有保护作用等。其具体机制还在继续研究中。 芪参益气滴丸能量代谢研究 结果显示：缺血（I/R）组ADP/ATP和AMP/ATP显著高于对照组，ATP 5D显著低于对照组，P-MLC显著高于对照组； 芪参益气滴丸+缺血（QSYQ）组ADP/ATP和AMP/ATP显著低于缺血组，ATP 5D显著高于缺血组，P-MLC显著低于缺血组； 芪参益气滴丸显著提高心肌组织ATP，显著改善心脏能量代谢水平 磷酸化肌球蛋白轻链[P-MLC，phosphorylate-myosin light chain]是Rho/ROCK通路下游的一个磷酸化产物,它可以促进肌动蛋白微丝骨架的聚合,引起细胞形态和功能的改变,进一步引起细胞收缩、游走、分裂、应力纤维产生及平滑肌运动、胶原合成等生物效应[3]。 3.3. Energy metabolism To address the energy metabolism in different conditions, we ?rst explored the ratio ADP/ATP and AMP/ATP in cardiac tissue. As shown in Fig. 3A and B, when compared with Sham group, QSYQ pre-treatment alone had no effect on either ADP/ATP or AMP/ATP. Of notice, I/R 90 min challenge dramatically increased ADP/ATP and AMP/ATP, to one and two fold Sham group, respectively, indicating a perturbation in the balance of energy metabolism inclining toward ATP catabolism. Interestingly, pre-treatment with QSYQ at 0.6 g/kg signi?cantly prevented both ADP/ATP and AMP/ATP from elevation by I/R 90 min. We next determined the expression of ATP 5D and ATP synthase α, two of the subunits of ATP synthase, in cardiac tissue in response to I/R 90 min, and the role of QSYQ in regulation of their expression. As shown in Fig. 3C2, the expression of ATP 5D reduced signi?cantly after I/R, as compared to Sham group. Pre-treatment with QSYQ at the dose of 0.6 g/kg signi?cantly restrained the decline of ATP 5D expression evoked by I/R. There was no notable variation in the expression of ATP synthase α among the four groups (Fig. 3C1). As one of the important effectors of ATP, the phosphorylation of MLC in various conditio