双参通冠方药物血清抗缺氧复氧损伤心肌细胞Ca^(2+)超载的机制研究

Mechanism of serum containing SSTG on calcium overload in cardiomyocytes injuryed by hypoxia and reoxygenation

目的:探讨双参通冠方药物血清对培养心肌细胞缺氧复氧损伤Ca2+超载的影响及其机制。方法:培养心肌细胞,建立缺氧复氧损伤模型。运用血清药理学方法研究双参通冠方药物血清对缺氧复氧损伤心肌Ca2+超载的影响。荧光分光光度法测定心肌细胞胞浆[Ca2+]i,激光扫描共聚焦显微法观察高K+及Thapsigargin诱导的细胞内Ca2+变化。结果:正常心肌细胞[Ca2+]i值较低,缺氧复氧后显著增高,高K+及Thapsigargin可诱导细胞内Ca2+的快速增多,双参通冠方药物血清能降低缺氧复氧心肌细胞Ca2+升高,并能抑制高K+及Thapsigargin所致的细胞内Ca2+荧光升高。结论:缺氧复氧损伤、高K+及Thapsigargin均可导致心肌细胞Ca2+增高,双参通冠方药物血清可抗心肌细胞Ca2+超载,其机制可能与其抑制细胞外Ca2+内流和促进内Ca2+吸收有关。

Objective： To explore the effects and mechanism of Shuangshen Tongguan （SSTG） serum, aformula composed of the acfive fractions of Chinese medicine, on calcium overload in cultured cardiomyocytes injured by hypoxia and reoxygenation, Method： The cardiomyocytes were deprived of oxygen and glucose to producl hypoxia reoxygenation injuried models. The changes of intracellular calcium fluorescence intensity induced by K^＋ and Thapsigzrgin were measured by fluorospectrophotometry and laster scanning confocal microscope respectively. Result： Intracellular calcium concentration was low in normal cardiomyocytes and was enhanced after hypoxia/reoxygenafion （ P 〈0. 05） ; SSTG drug serum reduced the intracellular calcium concentration and depressed the increase of calcium fluorescence intensity in singular cardiomyocyte due to K^＋ and Thapsigargin stimulation. Conclusion：Hypoxia/reoxygenafion injury, K^＋ and Thapsigargin could induce calcium overload in cardiomyocytes. The effects of calcium antagonism of SSTG drug serum were achieved by inhibiting calcium inflow, promoting calcium re-absorption of calcium.