摘要
目的 探讨辛伐他汀 (Simvastatin ,Sim)对血管升压素 (AVP)诱导的新生SD大鼠心脏成纤维细胞 (CFs)增殖的影响 ,为防治高血压心肌纤维化提供理论依据。方法 采用胰酶消化、差速贴壁法培养新生SD大鼠CFs,以3H 胸腺嘧啶核苷 (3H TdR)掺入法测定DNA合成、四氮唑盐 (MTT)比色法测定细胞数目 ,分别观察不同浓度Sim对AVP诱导CFs增殖的作用及甲羟戊酸 (Meval onate,MVA)干预的影响。结果 ①CFs(2 0 0个细胞 )的3H TdR掺入率随着Sim干预浓度的增加而降低 ,其中 1 0 - 6mol/LSim和 1 0 - 5mol/LSim组的3H TdR掺入率分别为 (1 1 75± 2 0 2 6 6 )、(771± 1 6 4 86 )cpm ,明显低于对照组 (1 95 5± 3 72 45 )cpm(P <0 0 1 ) ;②MTT比色法A490 值随Sim浓度的增加而降低 ,其中 1 0 - 6、1 0 - 5mol/LSim组的A490 值分别为 0 2 1 5± 0 0 4 1和 0 1 6 3± 0 0 1 8,均较对照组A490值 0 3 93± 0 0 4 8显著降低 (P <0 0 1 ) ;③ 1 0 - 5mol/LSim +1 0 - 3mol/LMVA组的3H TdR掺入率、MTT比色法A490 值分别为 (1 995±3 5 3 83 )cpm和 0 41 8± 0 0 4 5 ,均显著高于 1 0 - 5mol/LSim组 (P <0 0 1 )。结论 辛伐他汀可抑制AVP诱导的CFsDNA的合成和细胞数目增加 ,提示Sim可抑制CFs增殖 ,其机制可能通过甲?
Objective To investigate the effects of simvastatin (Sim) on the proliferation of rat cardiac fibroblasts (CFs) induced by arginine vasopressin (AVP) for theoretical bases of preventing and treating cardiac myofibrosis due to hypertention. Methods CFs of neonatal Sprague Dawley (SD) rats were isolated with trypsin digestion method and those growth arrested were stimulated with 10 -7 mol/L AVP in the presence of various concentrations of Sim and mevalonate (MVA). The DNA synthesis of CFs was measured with 3H Thymidine ( 3H TdR) incorporation. MTT colorimetry was adopted to evaluate cell number. Results ①Sim decreased 3H TdR incorporation in CFs in a concentration dependent manner. 3H TdR incorporation values of 10 -6 mol/L Sim and 10 -5 mol/L Sim group (1 175±202.66 and 771±164.86 cells in every 2 000 cells, respectively) were significantly lower than those of the control (1 955±372.45 in every 2 000 cells) (both P <0.01); ② A 490 values of 10 -6 mol/L Sim and 10 -5 mol/L Sim group (0.215±0.041, 0.163±0.018, respectively) were significantly lower than those of the control (0.393± 0.048) (both P < 0.01) . ③ 3H TdR incorporation in CFs and A 490 value of 10 -5 mol/L Sim+10 -3 mol/L MVA group (1 995±353.83 cells in every 2 000 cells, 0.418 ±0.045 respectively) were significantly higher in comparison with 10 -5 mol/L Sim group (both P <0.01). Conclusion The results indicate that Sim can decrease CFs number and DNA synthesis induce by AVP and MVA pathway may play an important role in the CFs proliferation.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2001年第12期1447-1449,共3页
Journal of Third Military Medical University