丹参酮ⅡA抑制氧化应激相关心肌肥大的研究

Study on tanshinone ⅡA in inhibiting oxidative stress related cardiac hypertrophy

目的探讨丹参酮ⅡA对氧化应激相关心肌肥大的改善作用及相关机制。方法采用不同浓度的丹参酮ⅡA处理心肌肥大细胞(5-羟色胺刺激诱导),观察其对细胞的表面积、合成速度、活性氧水平的影响,并采用Elisa法和RT-PCR检测Apelin和Apelin mR-NA水平。结果①与DMSO相比,丹参酮ⅡA可抑制5-羟色胺刺激诱导新生大鼠的心肌细胞表面积增大,且在30μmol/L浓度下效果最明显;②丹参酮ⅡA可降低心肌细胞的合成速度以及活性氧水平;③丹参酮ⅡA处理后Apelin和Apelin mRNA水平上升;④F13A(Apelin受体的拮抗剂)可减弱丹参酮ⅡA抑制心肌肥大的作用。结论丹参酮ⅡA可改善氧化应激相关的心肌肥大,可能的机制是通过上调Apelin而实现。

Objective It is to approach the improving effects of tanshinone Ⅱ A towards oxidative stress related cardiac hy- pertrophy and related mechanism. Methods The cell of cardiac hypertrophy model induced by 5 - hydroxytryptamine （5 - HT） was treated by different concentrations of tanshinone Ⅱ A. The following items were studied such as cell surface area, leucine incorporation and ROS. The ELISA and RT - PCR were employed to test the level of Apelin and Apelin mRNA. Re- sults （1）Compared with DMSO, the increased surface area of neonatal rat myocardial cells stimulated by 5 - HT serotonin with the significant effects at 30 μmol/L was inhibited by tanshinone Ⅱ A ; （2） The synthesis rate of protein and reactive oxygen spe- cies level were reduced by tanshinone ⅡA; （3） The levels of Apelin and Apelin mRNA were elevated after tanshinone Ⅱ A treatment; （4）The effect of tanshinone Ⅱ A in suppressing cardiac hypertrophy was reduced by the antagonist of Apelin receptor F13A. Conclusion Tanshinone Ⅱ A can improve oxidative stress related cardiac hypertrophy with possible mechanism of up- regulating Apelin.