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作 者:徐琳[1] 李志梁[1] 李高中[2] 刘映峰[1] 李公信[1] 丁明学[1] 赵霞[1]
机构地区:[1]南方医科大学珠江医院心脏内科,广东广州510280 [2]西安交通大学医院,陕西西安710061
出 处:《心脏杂志》2006年第2期190-193,共4页Chinese Heart Journal
摘 要:目的探讨辛伐他汀(S imvastatin,S im)对血管升压素(AVP)诱导的新生SD大鼠心脏成纤维细胞(CF)增殖和胶原合成作用的影响,为防治高血压左室肥厚提供理论依据。方法以培养的新生SD大鼠CF为实验模型,采用胰酶消化、差速贴壁法培养CF,运用MTT比色法和3H-脯氨酸掺入法分别观察不同浓度S im对AVP诱导CF增殖和胶原合成的作用及甲羟戊酸(m evalonate,MVA)干预的影响。结果①CF的3H-脯氨酸掺入率随着S im干预浓度的增加而降低,其中1μmol/L和10μmol/L S im组的3H-脯氨酸掺入率分别为(3.67±0.39)mBq/cell和(2.35±0.36)mBq/cell,明显低于对照组(5.01±0.58)mBq/cell(P<0.01);②MTT比色法A490值随S im浓度的增加而降低,其中1μmol/L和10μmol/L S im组的A490值分别为0.221±0.038和0.163±0.021,均较对照组A490值(0.395±0.039)显著降低(P<0.01);③10μmol/L S im+1 mmol/L MVA组的3H-脯氨酸掺入率和MTT比色法A490值分别为(5.38±0.72)mBq/cell和0.419±0.051,均显著高于同组10μmol/L S im(P<0.01)。结论S im抑制AVP诱导的CF增殖和胶原合成,其机制可能通过MVA代谢途径实现。AIM To investigate the effects of simvastatin (Sim) on the proliferation and collagen synthesis of rat cardiac fibroblasts (CF) induced by arginine vasopressin (AVP). METHODS CFs of neonatal Sprague-Dawley (SD) rats were isolated by trypsin digestion method and the growtH-arrested CFs were stimulated with 0.1 μmol/L AVP in the presence of varying concentrations of Sim (0.01 μmol/ L - 10 μmol/L) and MVA ( 1 μmol/L - 1 mmol/L). Collagen synthesis was measured by ^3H-proline incorporation and the cell number was evaluated by MTT. RESULTS The results showed that: ①Sim decreased ^3 H-proline incorporation in CFs in a concentration-dependent manner. ^3 H-proline incorporation values of 1 μmol/L Sim ^3H-proline group and 10 μmol/L Sim group (3.67 ±0.39 mBq/cell and 2.35 ±0.36 mBq/cell, respectively) were significantly lower than that of the control (5.01 ±0.58 mBq/cell,P 〈 0.01 ). ②The absorbance A490 values by MTT assay decreased with the elevation of Sim concentration. The A490 values of 1 μmol/L Sim group and 10 μmol/L Sim group (0.221 ±0.038, 0. 163 ±0.021, respectively) were significantly lower than that of the control (0. 395 ±0. 039, P 〈 0.01 ). ③^3H-proline incorporation in CFs and the A490 value of 10 ③mol/L Sim + 1 mmol/L MVA group (5.38 ±0.72 mBq/ cell and 0.419 ±0.051, respectively) were significantly higher compared with those of 10 μmol/L Sim group (P 〈0.01 ). CONCLUSION The results indicate that Sim decreases CF number and collagen synthesis induce by AVP and that MVA pathway may play an important role in the CF proliferation and collagen synthesis.
关 键 词:辛伐他汀 甲羟戊酸 心脏成纤维细胞 增殖 胶原合成
分 类 号:R544.1[医药卫生—心血管疾病]
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