体育科学
體育科學
체육과학
China Sport Science
2014年
5期
9~14
,共null页
运动 心脏重塑 miRNA-350 JNK 信号通路 动物实验 鼠
運動 心髒重塑 miRNA-350 JNK 信號通路 動物實驗 鼠
운동 심장중소 miRNA-350 JNK 신호통로 동물실험 서
exercise ; cardiac remodeling ; miRNA-350 ; JNK ; signaling pathway
目的:通过递增负荷跑台运动建立运动性心肌肥大模型,观察miRNA-350及其靶基因在8周递增负荷运动诱导的心脏重塑中的动态变化,以探讨运动心脏重塑的可能机制。方法:96只雄性C57BL/6小鼠随机分为对照组(C组)和递增负荷运动组(ILT组)。正式训练的第7周末,用超声心动图检测各组小鼠心脏结构和功能参数;用qRT-PCR检测运动心脏重塑过程中不同时相(0d、3d、7d、15d、29d和57d)miRNA-350的动态变化;分别用qRT—PCR和Western Blotting技术检测JNK mRNA和JNK蛋白的动态变化。结果:ILT组小鼠PWTS、PWTD、LVEDD、WSTD和WSTS等指标显著高于C组,EF无显著性差异;在运动心脏重塑过程中,ILT组小鼠心脏中miRNA-350的表达水平先快速增高再急剧下降,然后缓慢下降到与C组相当的水平;在递增负荷运动的0d、3d和7d,miRNA-350的靶基因JNKmRNA的表达水平没有显著变化,此后,JNKmRNA的表达水平呈上升趋势;在运动心脏重塑的初期,JNK蛋白的表达水平先显著下降再缓慢上升。结论:持续8周递增负荷跑台运动成功的诱导了小鼠心肌肥大;运动心脏重塑过程中miRNA-350、JNKmRNA和JNK蛋白呈动态变化,提示miRNA-350/JNK信号通路可能参与运动心脏重塑的调节。
目的:通過遞增負荷跑檯運動建立運動性心肌肥大模型,觀察miRNA-350及其靶基因在8週遞增負荷運動誘導的心髒重塑中的動態變化,以探討運動心髒重塑的可能機製。方法:96隻雄性C57BL/6小鼠隨機分為對照組(C組)和遞增負荷運動組(ILT組)。正式訓練的第7週末,用超聲心動圖檢測各組小鼠心髒結構和功能參數;用qRT-PCR檢測運動心髒重塑過程中不同時相(0d、3d、7d、15d、29d和57d)miRNA-350的動態變化;分彆用qRT—PCR和Western Blotting技術檢測JNK mRNA和JNK蛋白的動態變化。結果:ILT組小鼠PWTS、PWTD、LVEDD、WSTD和WSTS等指標顯著高于C組,EF無顯著性差異;在運動心髒重塑過程中,ILT組小鼠心髒中miRNA-350的錶達水平先快速增高再急劇下降,然後緩慢下降到與C組相噹的水平;在遞增負荷運動的0d、3d和7d,miRNA-350的靶基因JNKmRNA的錶達水平沒有顯著變化,此後,JNKmRNA的錶達水平呈上升趨勢;在運動心髒重塑的初期,JNK蛋白的錶達水平先顯著下降再緩慢上升。結論:持續8週遞增負荷跑檯運動成功的誘導瞭小鼠心肌肥大;運動心髒重塑過程中miRNA-350、JNKmRNA和JNK蛋白呈動態變化,提示miRNA-350/JNK信號通路可能參與運動心髒重塑的調節。
목적:통과체증부하포태운동건립운동성심기비대모형,관찰miRNA-350급기파기인재8주체증부하운동유도적심장중소중적동태변화,이탐토운동심장중소적가능궤제。방법:96지웅성C57BL/6소서수궤분위대조조(C조)화체증부하운동조(ILT조)。정식훈련적제7주말,용초성심동도검측각조소서심장결구화공능삼수;용qRT-PCR검측운동심장중소과정중불동시상(0d、3d、7d、15d、29d화57d)miRNA-350적동태변화;분별용qRT—PCR화Western Blotting기술검측JNK mRNA화JNK단백적동태변화。결과:ILT조소서PWTS、PWTD、LVEDD、WSTD화WSTS등지표현저고우C조,EF무현저성차이;재운동심장중소과정중,ILT조소서심장중miRNA-350적표체수평선쾌속증고재급극하강,연후완만하강도여C조상당적수평;재체증부하운동적0d、3d화7d,miRNA-350적파기인JNKmRNA적표체수평몰유현저변화,차후,JNKmRNA적표체수평정상승추세;재운동심장중소적초기,JNK단백적표체수평선현저하강재완만상승。결론:지속8주체증부하포태운동성공적유도료소서심기비대;운동심장중소과정중miRNA-350、JNKmRNA화JNK단백정동태변화,제시miRNA-350/JNK신호통로가능삼여운동심장중소적조절。
Objective:Cardiac hypertrophy model was induced by increasing load treadmill exer- cise, in order to observe the dynamic variation of miRNA-350 and target molecules in mice car- diac throughout a 8 week's increasing loading training, and explore the possibly mechanism of cardiac remodeling exercise training. Methods: 96 male C57BL/6 mice were randomly divided into 2 groups named control group and increasing load group. The cardiac structural and function parameters of all mice were determined by the ultrasonic cardiogram at the end of 7th week during the formal exercise training. The dynamic alternations of miRNA-350 during different time phases of cardiac remodeling induced to exercise training was determined by qRT- PCR. The dynamic expression of JNK mRNA and JNK protein was determined by qRT-PCR and Western Blotting technology. Results: There were significantly differences in the sizes of PWTS, PWTD, LVEDD, IVSTD and IVSTS between the C group and group ILT, but no difference in the eject fraction. At first, the expression of miRNA-350 in the cardiac of ILT group presented a sharp ascent and followed an acute decline, and then slowly down to a level similar to C group. At the day of 0,3 and 7 throughout increasing load training period, the expression of JNK mRNA, target gene of miRNA-350 had no remarkable change. Since then the expression level of JNK mRNA increased gradually. The expression of JNK protein decreased dramatically and then increased slowly in the course of cardiac remodeling induced by exercise. Conclusions:It indicated that a lasting 8 weeks' increasing load treadmill exercise training induced a cardiac hypertrophy successfully. It appeared that the expression of miRNA-350,JNK mRNA and JNK protein showed a dynamic alternations during exercise-induced cardiac remodeling, and implied that miRNA-350/JNK signaling pathways possibly involved in the regulation of exercise-induced cardiac remodeling.