基础医学与临床 ›› 2017, Vol. 37 ›› Issue (3): 346-350.

• 研究论文 • 上一篇    下一篇

辛伐他汀对血管紧张素II刺激的肾上腺皮质癌H295R细胞的分泌和增殖的影响

李春艳1,2,童安莉2,王芬2,崔云英3,闫朝丽4   

  1. 1. 内蒙古医科大学 附属医院
    2. 中国医学科学院北京协和医学院北京协和医院内分泌科 卫生部内分泌重点实验室
    3. 中国医学科学院北京协和医院内分泌科卫生部内分泌重点实验室
    4. 内蒙古医科大学 第一附属医院
  • 收稿日期:2016-11-28 修回日期:2016-12-18 出版日期:2017-03-05 发布日期:2017-02-23
  • 通讯作者: 童安莉 E-mail:tonganli@hotmail.com
  • 基金资助:
    国家临床重点专科

Effect of simvastatin on angiotensin II-stimulated secretion and proliferation of adrenocortical carcinoma H295R cells

  • Received:2016-11-28 Revised:2016-12-18 Online:2017-03-05 Published:2017-02-23
  • Contact: TONG An-li E-mail:tonganli@hotmail.com

摘要: 目的 研究辛伐他汀对血管紧张素II(Ang II)刺激的肾上腺皮质癌H295R细胞的分泌和增殖的影响。方法 H295R细胞分为对照组、Ang II(100 nmol/L)处理组、辛伐他汀(10 μmol/L)处理组和Ang II+辛伐他汀处理组,用化学发光法检测培养液中的皮质醇;用放射免疫分析法(RIA)检测培养液中的醛固酮;用实时荧光定量聚合酶链反应检测11β-羟化酶(CYP11B1)和醛固酮合成酶(CYP11B2)的mRNA表达;用MTS法观察细胞增殖。结果 与对照组相比,Ang II刺激皮质醇和醛固酮分泌及其合成酶CYP11B1与CYP11B2 mRNA的表达,辛伐他汀抑制皮质醇分泌及其合成酶CYP11B1 mRNA的表达(P < 0.05);与单独Ang II处理组相比,Ang II+辛伐他汀组能显著抑制Ang II刺激的皮质醇和醛固酮分泌及其合成酶CYP11B1与CYP11B2 mRNA的表达(P< 0.05);Ang II对H295R细胞增殖无明显影响,辛伐他汀抑制细胞增殖,并且,辛伐他汀与Ang II联合处理细胞,这种抑制作用更显著 (P< 0.05)。结论 辛伐他汀抑制Ang II诱导的肾上腺皮质癌H295R细胞的皮质醇与醛固酮的分泌;辛伐他汀抑制H295R细胞增殖,与Ang II联合处理细胞这种抑制作用更显著。

关键词: 辛伐他汀, 血管紧张素II, H295R细胞, 分泌功能, 细胞增殖

Abstract: Objective To investigatethe potential effects of simvastatin on angiotensin II-stimulatedsecretion and proliferation of adrenocortical carcinoma H295R cells. Methods The H295R cells were divided into control group, Angiotensin II group, simvastatin group and Angiotensin II plus simvastatin group. Cortisol in medium was determined by chemiluminescent method, and aldosterone was determined by radioimmunoassay. The mRNA expressions of 11 beta-hydroxylase(CYP11B1) and aldosterone synthase(CYP11B2) were examined by real-time quantitative PCR. Cell proliferation was detected by MTS method. Results Compared with control group, angiotensin II increased the secretion of cortisol and aldosterone, and the expression of CYP11B1 and CYP11B2. Simvastatin decreased cortisol secretion and CYP11B1 mRNA expression (P < 0.05). Simvastatin also inhibited angiotensin II-induced the secretion of cortisol and aldosterone, and the expression of CYP11B1 and CYP11B2 compared with Angiotensin II group(P < 0.05). Angiotensin II had no effects on the cell proliferation, while simvastatin significantlyinhibited cell proliferation. The inhibitory effect of simvastatin on proliferation was enhanced when simvastatin combined with angiotensin II(P < 0.05). Conclusions Simvastatin can inhibit angiotensin II-induced secretion of cortisol and aldosterone in H295R cells. Simvastatin inhibits cell proliferation, which could be enhanced by simvastatin combined with angiotensin II.

Key words: simvastatin, angiotensin II, H295R cell, secretion function, cell proliferation

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