北京体育大学学报
北京體育大學學報
북경체육대학학보
Journal of Beijing University of Physical Education
2014年
5期
77~83
,共null页
游泳运动 心衰 miRNA-350 JNK 信号通路 小鼠
遊泳運動 心衰 miRNA-350 JNK 信號通路 小鼠
유영운동 심쇠 miRNA-350 JNK 신호통로 소서
swimming ; heart failure ; miRNA - 350 ; JNK ; signaling pathway ; mice
目的：建立颈动脉缩窄术心衰小鼠模型，观察长期游泳运动对心衰小鼠左心室miRNA-350及其靶基因JNK表达的影响，以探讨有氧运动改善心脏疾病的可能机制。方法：雄性C57BL／6小鼠分为对照组（c组，n=8只）、心衰模型组（HFM组，n=8只）和心衰模型运动组（HFME组，n=8只）。超声心动图仪检测各组小鼠心脏形态和功能参数；分别用qRT-PCR和Western Blotting技术检测各组小鼠左心室miR-NA-350、JNK mRNA和JNK蛋白的表达水平。结果：TAC手术后28 d时，HFM组和HFME组PWTS、PWTD、LVEDD、IVSTD和IVSTS显著高于c组，EF显著低于c组。取材前1周，HFM组和HFME组PWTS、PWTD、LVEDD、IVSTD和IVSTS等显著高于C组，EF显著低于c组；HFME组LVEDD和EF显著高于HFM组。末次训练后，HFM组左心室miRNA-350表达水平显著高于c组，HFME组左心室miRNA-350表达水平显著低于HFM组，但明显高于c组；HFME组左心室JNK mRNA表达水平显著高于c组和HFM组；HFME组左心室JNK蛋白表达水平虽明显高于HMF组，但显著低于c组。结论：TCC手术成功复制了心衰小鼠模型，表现为PWTS、PWTD、LVEDD、IVSTD和IVSTS显著增厚和EF显著降低。运动改善小鼠心衰表征的机制可能与运动抑制miRNA-350的表达，进而增强JNK mRNA和JNK蛋白的表达有关。
目的：建立頸動脈縮窄術心衰小鼠模型，觀察長期遊泳運動對心衰小鼠左心室miRNA-350及其靶基因JNK錶達的影響，以探討有氧運動改善心髒疾病的可能機製。方法：雄性C57BL／6小鼠分為對照組（c組，n=8隻）、心衰模型組（HFM組，n=8隻）和心衰模型運動組（HFME組，n=8隻）。超聲心動圖儀檢測各組小鼠心髒形態和功能參數；分彆用qRT-PCR和Western Blotting技術檢測各組小鼠左心室miR-NA-350、JNK mRNA和JNK蛋白的錶達水平。結果：TAC手術後28 d時，HFM組和HFME組PWTS、PWTD、LVEDD、IVSTD和IVSTS顯著高于c組，EF顯著低于c組。取材前1週，HFM組和HFME組PWTS、PWTD、LVEDD、IVSTD和IVSTS等顯著高于C組，EF顯著低于c組；HFME組LVEDD和EF顯著高于HFM組。末次訓練後，HFM組左心室miRNA-350錶達水平顯著高于c組，HFME組左心室miRNA-350錶達水平顯著低于HFM組，但明顯高于c組；HFME組左心室JNK mRNA錶達水平顯著高于c組和HFM組；HFME組左心室JNK蛋白錶達水平雖明顯高于HMF組，但顯著低于c組。結論：TCC手術成功複製瞭心衰小鼠模型，錶現為PWTS、PWTD、LVEDD、IVSTD和IVSTS顯著增厚和EF顯著降低。運動改善小鼠心衰錶徵的機製可能與運動抑製miRNA-350的錶達，進而增彊JNK mRNA和JNK蛋白的錶達有關。
목적：건립경동맥축착술심쇠소서모형，관찰장기유영운동대심쇠소서좌심실miRNA-350급기파기인JNK표체적영향，이탐토유양운동개선심장질병적가능궤제。방법：웅성C57BL／6소서분위대조조（c조，n=8지）、심쇠모형조（HFM조，n=8지）화심쇠모형운동조（HFME조，n=8지）。초성심동도의검측각조소서심장형태화공능삼수；분별용qRT-PCR화Western Blotting기술검측각조소서좌심실miR-NA-350、JNK mRNA화JNK단백적표체수평。결과：TAC수술후28 d시，HFM조화HFME조PWTS、PWTD、LVEDD、IVSTD화IVSTS현저고우c조，EF현저저우c조。취재전1주，HFM조화HFME조PWTS、PWTD、LVEDD、IVSTD화IVSTS등현저고우C조，EF현저저우c조；HFME조LVEDD화EF현저고우HFM조。말차훈련후，HFM조좌심실miRNA-350표체수평현저고우c조，HFME조좌심실miRNA-350표체수평현저저우HFM조，단명현고우c조；HFME조좌심실JNK mRNA표체수평현저고우c조화HFM조；HFME조좌심실JNK단백표체수평수명현고우HMF조，단현저저우c조。결론：TCC수술성공복제료심쇠소서모형，표현위PWTS、PWTD、LVEDD、IVSTD화IVSTS현저증후화EF현저강저。운동개선소서심쇠표정적궤제가능여운동억제miRNA-350적표체，진이증강JNK mRNA화JNK단백적표체유관。
Objective： This study established heart failure model of mice by carotid artery coaretation and observed the effects of long-term swimming on expressions of miRNA - 350 and JNK gene, in order to explore the mechanism of im proving heart disease by aerobics. Methods： Twenty-four male C57BL/6 rats were divided into control group （ C, n = 8）, heart failure model group （HFM, n =8） and heart failure model combined exercise/swimming （HFME, n =8） The morphological and functional parameters of heart were measured by eehocardiogram. The expressions of miRNA - 350, JNK mRNA and JNK protein were determined by qRT-PCR and western blotting, Results： PWTS, PWTD, LVEDD, IVSTD, IVSTS in HFM group and HFME group are higher than in C group, and EF is lower than in C group, 28 days after carotid artery coarctation and one week before last day. Also LVEDD and EF in HFME group are higher than in HFM group one week before last day. Left ventricle＇ s rniRNA - 350 expression in HFM group is higher than in HFME and C groups after training, and it in HFME group is higher than in C group. JNK mRNA expression of left ventricle in HFME group is higher than in C and HFM groups. JNK protein expression of left ventricle in HFME group is lower than in I-IFM group, but higher than in C group. Conclusion： Carotid artery eoaretation established heart failure model of mice, which characterized by increases of PWIX3, PWTD, LVEDD, IVSTD and decline of EF. The mechanism of the fact that exercise can imorove heart disease is that exercise can inhibit the expression of miRNA -350 and en-hance mRNA and protein expressions of JNK.
