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【目的】研究蕨麻正丁醇部位对大鼠心肌细胞缺氧所致钙超载的抑制作用,并通过研究其对心肌细胞L-型钙通道(Ltype calcium channel,Cav1.2)及肌浆网兰尼定受体(Ryanodine receptor,Ry R)表达的影响,探讨其可能的机制。【方法】建立原代心肌细胞缺氧模型,设正常对照组、缺氧损伤组、维拉帕米组(5μmol/L)及蕨麻正丁醇部位高、中、低浓度组(250.0、62.5、15.6μg/ml)。采用荧光分光光度法检测各组心肌细胞内钙离子变化,RT-PCR法检测心肌细胞Cav1.2和Ry R m RNA表达水平。【结果】缺氧损伤组心肌细胞内游离钙离子的浓度较正常对照组明显增加(P<0.01),Cav1.2 m RNA、Ry R m RNA表达明显增强(P<0.01),维拉帕米组和蕨麻正丁醇部位高、中、低浓度组心肌细胞内游离钙离子的浓度较缺氧损伤组明显降低,Cav1.2 m RNA(P<0.01或P<0.05)和Ry R m RNA(P<0.01)表达明显降低。【结论】蕨麻正丁醇部位可明显抑制缺氧所致心肌细胞钙超载,抑制L-型钙通道和Ry R的表达。提示蕨麻正丁醇部位抑制心肌细胞内钙超载的作用可能与其抑制L型钙通道有关。
【Objective】 To study the inhibitory effect of n-butanol fraction on calcium overload caused by hypoxia in rat cardiomyocytes, and to study its effects on L-type calcium channel (Cav1.2) and sarcoplasmic reticulum Ryanodine receptor (RyR) expression, explore its possible mechanism. 【Methods】 The primary hypoxic model of cardiomyocytes was established. The normal control group, hypoxic injury group, verapamil group (5μmol / L) , 15.6 μg / ml). The changes of intracellular calcium in each group were detected by fluorescence spectrophotometry. The expression of Cav1.2 and Ry R m RNA in myocardial cells were detected by RT-PCR. 【Results】 The results showed that the concentration of intracellular free calcium in myocardial cells in hypoxia group was significantly higher than that in normal control group (P <0.01), Cav1.2 m RNA and Ry R m RNA were significantly increased (P <0.01) (P <0.01 or P <0.05) and Ry R m RNA (P <0.01 or P <0.05). Compared with hypoxia group, the concentration of free calcium in myocardial cells of high, (P <0.01), the expression was significantly reduced. 【Conclusion】 The n-butanol fraction significantly inhibited the calcium overload of cardiomyocytes induced by hypoxia, and inhibited the expression of L-type calcium channel and Ry R. It is suggested that the effect of nimotetine on inhibition of calcium overload in myocardial cells may be related to the inhibition of L-type calcium channel.