双参通冠方药物血清抗缺氧复氧损伤心肌细胞Ca2+超载的机制研究

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。

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

Objective: To explore the effects and mechanism of Shuangshen Tongguan(SSTG) serum,a formula composed of the active 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 Thapsigargin were measured by fluorospectrophotometry and laster scanning confocal microscope respectively.Result: Intracellular calcium concentration was low in normal cardiomyocytes and was enhanced after hypoxia/reoxygenation(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/reoxygenation 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.