摘要
目的探讨川芎嗪(tetramethylpyrazine,TMP)抑制血管紧张肽Ⅱ(AngⅡ)诱导心肌细胞肥大的作用机制。方法应用细胞培养技术培养新生大鼠心肌细胞,应用AngⅡ刺激培养的心肌细胞制作肥大心肌细胞模型,采用相差显微镜测量细胞大小及测定心肌细胞3H-亮氨酸掺入作为心肌细胞肥大的指标;fura-3/AM孵育心肌细胞,利用荧光显微镜及Felix软件分析测定细胞内钙离子浓度([Ca2+]i);Western blot检测钙调神经磷酸酶(calcineurin,CaN)蛋白表达。结果与正常对照组比较,AngⅡ组心肌细胞明显肥大(P<0.01),3H-亮氨酸掺入量明显增加(P<0.01),川芎嗪+AngⅡ组心肌细胞肥大及3H-亮氨酸掺入量明显抑制(均P<0.01),与氯沙坦+AngⅡ组差异无显著性。AngⅡ组较对照组细胞内Ca2+浓度及CaN蛋白表达明显升高(P<0.01或P<0.05),川芎嗪+AngⅡ组较AngⅡ组Ca2+浓度及CaN蛋白表达则受到明显抑制(P<0.01或P<0.05),氯沙坦+AngⅡ组与川芎嗪+AngⅡ组差异无显著性。结论川芎嗪能明显抑制心肌细胞肥大,其机制与干预Ca2+/CaN信号转导通路有关。
Objective To study the interference effect and mechanism of tetramethylpyrazine （TMP） on myocardiac hypertrophy induced by angiotensin Ⅱ（ Ang Ⅱ）. Methods The cardiomyocyte hypertrophy cell model was induced by stimulating with angiotensinⅡ （ Ang Ⅱ） in vitro ; The cell size was determined by phase contrast microscope and ^3 H-leucine incorporation were investigated; the concentration of Ca^2＋ was determined by fura-3/AM fluorescent technique ; the protein expression of CaN was measured by Western blot. Results After treatment with Ang Ⅱ , the cell size ,^3 H-leucine incorporation rate, [ Ca^2＋ ] i and the protein expression of CaN were increased significantly（ P 〈 0.01, P 〈 0.05 ）. Being treated with TMP, all indexes were obviously reduced by comparing with Ang Ⅱ group（ P 〈 0.01, P 〈 0.05 ）, which were similar to losartan group. Conclusion TMP can prevent the cardiac hypertrophy and the mechanism could be related to interference on Ca^2＋/CaN signal pathway.
出处
《医药导报》
CAS
2009年第10期1265-1268,共4页
Herald of Medicine
