S-亚硝基谷胱甘肽对PGF2α诱导心肌肥大的抑制作用  

S-nitrosoglutathione inhibits cardiaomyocyte hypertrophy induced by prostaglandin F2α

作　　者：邱红梅[1] 

机构地区：[1]重庆医科大学药理教研室,400016

出　　处：《重庆医学》2009年第18期2304-2305,2307,F0002,共4页Chongqing medicine

摘　　要：目的从细胞水平研究一氧化氮(Nitric oxide,NO)供体S-亚硝基谷胱甘肽(S-nitrosoglutathione,GSNO)对前列腺素F2α(PGF2α)所致心肌肥大的影响,并初步探讨其作用原理。方法利用培养的新生大鼠心肌细胞,以细胞直径大小、蛋白质含量为心肌肥大反应指标,观察药物的抗心肌肥大效应;分别用比色法和荧光法检测细胞NO浓度和游离钙浓度(〔Ca2+〕i),分析其可能的作用原理。结果PGF2α10-7mol/L使心肌细胞明显增大,蛋白质含量明显增加,并使〔Ca2+〕i显著升高,但对NO含量无明显影响。与PGF2α组比较,GSNO10-4mol/L明显使心肌细胞直径、蛋白质含量和〔Ca2+〕i减少;同时使NO浓度明显增加,差异有统计学意义(P<0.05)。结论GSNO可抑制PGF2α诱导的心肌细胞肥大,该作用可能与其释放NO,使心肌细胞局部NO含量增加,从而降低细胞内钙有关。Objective To observe the effects of S-nitrosoglutathione（GSNO）on cardiac myocyte hypertrophy induced by prostaglandin F2α （PGF2α） ,and to probe primarily its mechanisms. Methods Neonatal rat cardiomyocyte hypertrophic response and the antihypertrophic effects of GSNO were assayed by measuring cell diameter and protein content. The nitric oxide （NO） concentration and the intracellular free calcium concentration （ [Ca^2＋ ]i ） in cultured cardiornyoeytes were measured by colorirnetry or by using Fura 2/AM as a fluorescent indicator,respectively. Results PGF2α at 10^-7mol/L significantly increased the cell diameter,protein content and [Ca^2- ]i in cultured cardiornyocyte, but had no effects on NO release. GSNO at 10 ^-4mol/L could significantly inhibit the cardiornyocyte hypertrophy induced by PGF2α. Oppositely, NO release was reduced by GSNO（P〈0.05）. Similarly, [Ca^2＋ ]i was reduced by GSNO. Conclusion Cardiomyocyte hypertrophyic response could be abolished by GSNO partly,which may be related to its effects on the increase the release of NO and then inhibiting the increase of [Ca^2- ]i induced by PGF2α.

关 键 词：S-亚硝基谷胱甘肽 前列腺素F2Α 心肌肥大 一氧化氮 钙 

分 类 号：R541[医药卫生—心血管疾病]