摘要
目的:探讨过氧化物酶体增殖物激活型受体(PPARs)配体对血管紧张素Ⅱ(AngⅡ)诱导心脏成纤维细胞(CFs)增殖的影响及其机制。方法:体外传代培养乳鼠CFs,分别以非诺贝特(PPARα配体)和(或)吡格列酮(PPARγ配体)预处理24h后,加用AngⅡ刺激诱导CFs增殖。应用流式细胞仪分析细胞周期,以MTT比色法测定心肌细胞活力,反映细胞增殖及胶原合成。结果:与对照组比较,非诺贝特、吡格列酮均降低AngⅡ诱导的CFs的S期细胞比率和增殖指数,抑制AngⅡ引起细胞活力改变和增殖(P<0.01)。相对单独用药组,2药合用组的上述指标差异无统计学意义(P>0.05)。结论:PPARs信号通路激活能有效抑制AngⅡ诱导的CFs增殖,预防心肌纤维化。PPARα、γ配体合用未见明显叠加效应。
Objective：To investigate the effects of peroxisome proliferator-activated receptors （PPARs） α and γ ligands （fenofibrate and pioglitazone） on the angiotensin Ⅱ （AngⅡ）-induced cardiac fibroblasts （CFs） proliferation and collagen synthesis. Method：CFs of neonatal rat were obtained by enzymatic dissociation and then Ang Ⅱ was used to stimulate CFs proliferation. Fenofibrate and pioglitazone had been pretreated for 24 h prior to Ang Ⅱ. Cell cycle kinetics of CFs was analyzed by flow cytometry. CFs viability was estimated by MTT assay. Result： Ang Ⅱ increased the S-phase fraction, proliferation index and viability of CFs （P〈0.01）. Pretreatment of fenofibrate or pioglitazone significantly reduced the effects of Ang Ⅱ-induced CFs （P〈0.01）. There were no significant differences in the above mentioned indices in fenofibrate and pioglitazone combined group （P〉0.05）. Conclusion： PPARs-ligands （fenofibrate and pioglitazone） might attenuate myocardial fibrosis induced by Ang Ⅱ through inhibiting the CFs proliferation. There is no additive effect by combining the two drugs.
出处
《临床心血管病杂志》
CAS
CSCD
北大核心
2007年第8期594-596,共3页
Journal of Clinical Cardiology
基金
贵州省科技攻关项目(No:黔科合2004NGY043)
