人参皂苷Rb1对肺动脉高压大鼠钙库操纵性钙内流的影响

Effect of ginsenoside Rb1 on store-operated calcium entry in rats with pulmonary hypertension

  • 摘要: 目的:观察在体人参皂苷Rb1预处理对慢性低氧(CH)肺动脉高压大鼠肺动脉平滑肌细胞钙库操纵性钙内流(SOCE)的影响。方法:将30只雄性SD大鼠随机分为正常对照组(control组)、CH肺动脉高压模型组(CH组)和Rb1(30 mg/kg)组,每组10只。检测各组右心室收缩压、右心室质量指数和肺动脉血管环张力。体外培养大鼠肺动脉平滑肌细胞,采用细胞动态荧光检测游离Ca2+浓度。分别采用实时荧光定量PCR(RT-qPCR)和western blotting检测基质相互作用分子2(STIM2)和钙释放激活钙调节因子2(Orai2)基因和蛋白表达。结果:与CH组比较,Rb1组大鼠右心室收缩压和右心室质量指数均明显降低(P<0.01),环匹阿尼酸(CPA)诱发的肺动脉收缩张力和钙内流量明显减少(P<0.01),STIM2和Orai2 mRNA和蛋白相对表达量明显降低(P<0.05)。结论:Rb1可明显改善CH肺动脉高压大鼠的肺动脉压,其作用机制可能与减弱肺动脉SOCE功能和STIM2和Orai2表达有关。

     

    Abstract: Objective: To observe the effect of pretreatment with ginsenoside Rb1 in vivo on store-operated calcium entry(SOCE) in pulmonary artery smooth muscle cells of rats with chronic hypoxia(CH) pulmonary hypertension. Methods: Thirty male SD rats were randomly divided into normal control group(control group), CH pulmonary hypertension model group(CH group) and Rb1(30 mg/kg) group, with 10 rats in each group. The right ventricular systolic pressure, right ventricular mass index, and pulmonary artery vascular tension in each group were measured. The pulmonary artery smooth muscle cells of rats were cultured in vitro, and the free Ca2+concentration was detected by cell dynamic fluorescence. The gene and protein expressions of stromal interaction molecule 2(STIM2) and calcium release-activated calcium modulator 2(Orai2) were detected by real-time quantitative PCR(RT-qPCR) and western blotting. Results: Compared with the NC group, the right ventricular systolic pressure and right ventricular mass index of the rats in the Rb1 group were significantly lower(P<0.01), the cyclopiazonic acid(CPA)-induced pulmonary artery constriction tension and intracellular calcium influx were significantly reduced(P<0.01), and STIM2, Orai2 mRNA as well as protein expression of relative amount were significantly decreased(P<0.05).Conclusion: Rb1 can significantly improve the pulmonary artery pressure in CH rats with pulmonary hypertension, and the mechanism may be related to the reduction of SOCE function and the expression of STIM2 and Orai2 in pulmonary artery.

     

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