【摘要】 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。更多还原

【Abstract】 Objective It is to approach the improving effects of tanshinone ⅡA towards oxidative stress related cardiac hypertrophy and related mechanism.Methods The cell of cardiac hypertrophy model induced by 5-hydroxytryptamine(5-HT) was treated by different concentrations of tanshinone ⅡA.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.Results ①Compared 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 ⅡA;② The synthesis rate of protein and reactive oxygen species level were reduced by tanshinone ⅡA;③ The levels of Apelin and Apelin mRNA were elevated after tanshinone ⅡA treatment;④The effect of tanshinone ⅡA in suppressing cardiac hypertrophy was reduced by the antagonist of Apelin receptor F13A.Conclusion Tanshinone ⅡA can improve oxidative stress related cardiac hypertrophy with possible mechanism of up-regulating Apelin.更多还原