CAJ | 학술논문

目的：观察PPAR-γ激动剂罗格列酮对内皮素-1（ET-1）诱导心肌肥大的作用，并探讨PPAR-γ激活后抑制心肌肥厚的机制。方法：采用[3H]亮氨酸掺入法、逆转录聚合酶链式反应（RT-PCR）、蛋白免疫印迹（Western blot）等实验方法，观察罗格列酮对ET-1诱导培养新生SD大鼠心肌细胞肥大的作用，罗格列酮对ET-1诱导的心肌细胞钙调神经磷酸酶（calcineurin ）活性、mRNA及蛋白表达增加的影响。结果：罗格列酮可显著抑制ET-1所致心肌细胞蛋白合成增加、肥大基因表达、Calcineurin酶活性增高、mRNA及蛋白表达增加（P＜0.01），该作用可被PPAR-γ受体拮抗剂GW9662逆转（P＜0.01）。结论：ET-1可通过激活calcineurin信号通路诱导心肌肥厚，罗格列酮以PPAR-γ依赖的方式抑制calcineurin信号通路，防止心肌肥大发生。
목적：관찰PPAR-γ격동제라격렬동대내피소-1（ET-1）유도심기비대적작용，병탐토PPAR-γ격활후억제심기비후적궤제。방법：채용[3H]량안산참입법、역전록취합매련식반응（RT-PCR）、단백면역인적（Western blot）등실험방법，관찰라격렬동대ET-1유도배양신생SD대서심기세포비대적작용，라격렬동대ET-1유도적심기세포개조신경린산매（calcineurin ）활성、mRNA급단백표체증가적영향。결과：라격렬동가현저억제ET-1소치심기세포단백합성증가、비대기인표체、Calcineurin매활성증고、mRNA급단백표체증가（P＜0.01），해작용가피PPAR-γ수체길항제GW9662역전（P＜0.01）。결론：ET-1가통과격활calcineurin신호통로유도심기비후，라격렬동이PPAR-γ의뢰적방식억제calcineurin신호통로，방지심기비대발생。
To tested the hypothesis that rosiglitazone exerted negative effects on cardiac hypertrophy in PPAR-γ-dependent manner . Methods:[ 3H ] leucine incorporation assay was performed to measure protein synthesis . RT-PCR analysis and Western-blot analysis were performed to analyze the effects of rosiglitazone on ET-1-induced calcineurin mRNA level and protein expression . Results:ET-1 treatment markedly increased protein synthesis , ANF mRNA expression , calcineurin enzyme activity , calcineurin mRNA and protein expression (P<0 . 01). Treatment with rosiglitazone inhibited these effects and were reversed by PPAR-γ antagonist GW9662 (P<0 . 01). Conclusion: ET-1 may induce cardiac hypertrophy through activating of the calcineurin pathway . Rosiglitazone abrogate cardiac hypertrophy via the calcineurin pathway in a PPAR-γ-dependent way .