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目的考察双参通冠方(SSTG)药物血清对缺氧/复氧心肌细胞Ca2+-CaM-CaMPKⅡ信号系统的影响。方法培养心肌细胞,建立缺糖缺氧/复氧损伤模型。运用血清药理学方法研究SSTG药物血清对缺糖缺氧/复氧损伤心肌的作用。荧光分光光度法测定心肌细胞胞质[Ca2+]i,RT-PCR法测定CaM、CaMPKⅡδmRNA表达。结果正常心肌细胞[Ca2+]i、CaM、CaMPKⅡδmRNA表达很低。缺氧/复氧后[Ca2+]i较正常组增高,CaM、CaMPKⅡδmRNA表达增高(P<0.05),SSTG提取物大鼠灌胃剂量为22.5、45、90 mg.kg-1所取得的药物血清(体积分数为0.1)处理组[Ca2+]i降低,CaM、CaMPKⅡδmRNA表达降低,与空白血清处理组相比差异有统计学意义(P<0.05)。结论缺氧/复氧损伤可导致心肌细胞Ca2+超载,CaM、CaMPKⅡδmRNA表达增高;SSTG药物血清可对抗心肌细胞Ca2+超载,抑制其胞内受体CaM及Ca2+/CaM依赖性蛋白激酶CaMPKⅡδ的活性。
Objective To investigate the effect of SSTG serum on Ca2+-CaM-CaMPKII signaling system in hypoxia/reoxygenation cardiomyocytes. Methods Cardiomyocytes were cultured and hypoxia/hypoxia/reoxygenation injury models were established. Serum pharmacological methods were used to study the effect of serum of SSTG on myocardial injury induced by hypoxia/hypoxia/reoxygenation injury. The cytoplasmic [Ca2+]i of myocardial cells was measured by fluorescence spectrophotometry. The expression of CaM and CaMPKIIδ mRNA was determined by RT-PCR. Results The expression of [Ca2+]i, CaM, CaMPKIIδ mRNA in normal myocytes was very low. After hypoxia/reoxygenation, [Ca2+]i increased compared with normal group, CaM and CaMPKIIδ mRNA expression increased (P<0.05), SSTG extract rats received intragastric administration doses of 22.5, 45, and 90 mg.kg-1. In the treatment group, [Ca2+]i decreased, CaM, CaMPKIIδ mRNA expression decreased, and the difference was statistically significant (P<0.05). Conclusion Hypoxia/reoxygenation injury can lead to Ca2+ overload and CaM, CaMPKIIδ mRNA expression in myocardial cells. Serum of SSTG can inhibit Ca2+ overload of cardiomyocytes and inhibit the activity of CaM and Ca2+/CaM-dependent protein kinase CaMPKIIδ.