| Objective:This article shows that the influence of miR-29a/TGF-β1/Smad2/3and miR-101a/c-Fos/TGF-β1pathway and the relationship with MI myocardial fibrosis that intermittent aerobic exercise caaused and investigates the mechanism that intermittent aerobic exercise can degrade cardiac fibrosis.Method:The48male3-month-old SD rats were randomly divided into four groups, including two groups of myocardial infarction (MI) surgery and the other two groups that received sham surgery (Sham,wearing lines,without ligation).The four groups:MI sedentary group (MI group), sham+sedentary group (S group), MI+intermittent aerobic exercise group (ME group), sham+intermittent aerobic exercise group (SE group). The exercise load of intermittent aerobic exercise groups was based on slightly altered Wisl(?)ff training model:1wk after MI, for1wk adaptive training (15m/min,30min/d×5d),40%～50%VO2max warm-up (10m/min×10min),85%～90%VO2max (25m/min×7min) and50%～60%VO2max (15m/min×3min) intermittent aerobic exercise and turned alternately. The total time was60min,5d/wk,8w.The rat models of MI were established by adopting the left anterior descending coronary artery ligation (LAD). By using the right common carotid artery to the left ventricle in rats haemodynamics parameters were measured. Combined with ECG cardiac function in rats was evaluated.The fibrosis area of myocardial infarction and the extent of myocardial hypertrophy in non-infarcted part were calculated by paraffin section and masson staining and microscopic image analysis system. By the real-time PCR the expression of miR-29a and miR-101a were determined and by the Western Blot method pathway proteins and their characterizations of COL1A1, COL3A1, TGFβ-1/Smad2/3and c-Fos/TGFβ-1were determined.Result:1Intermittent aerobic exercise can significantly increase the degree of myocardial hypertrophy, myocardial COL1A1and COL3A1reduced significantly. It was showed that intermittent aerobic exercise can reduce myocardial fibers and interstitial collagen synchronously and improve heart function significantly. 2MI induced excessive accumulation of myocardial collagen, myocardial fibrosis and cardiac dysfunction. Intermittent aerobic exercise can reduce myocardial fibrosis and improve cardiac function.3After MI myocardial collagen was metabolic imbalance, excessive accumulation of collagen fibers, and the expression of COL1A1and COL3A1significantly increased. Intermittent aerobic exercise can significantly reduce the expression of COL1A1and COL3A1and myocardial fibrosis.4Intermittent aerobic exercise can significantly elevate expression of miR-29a and reduce protein expression of TGF-β1/Smad2/3in normal rat heart. Intermittent aerobic exercise that elevated cardiac miR-29a expression plays an important role in the regulation of synchronous development of myocardial collagen hyperplasia and myocardial fibers hypertrophy.5Intermittent aerobic exercise can significantly reduce myocardial local protein content of TGF-β1/Smad2/3in MI rats and degrade myocardial fibrosis.6MI significantly reduced expression of miR-29a in rat myocardium and intermittent aerobic exercise can significantly elevate expression of miR-29a in myocardial local of MI rat and TGF-β1/Smad2/3signaling pathway plays a role in degrading myocardial fibrosis of the MI rats.7Intermittent aerobic exercise can significantly elevate expression of miR-101a and reduce protein expression of c-Fos/TGF-β1in normal rat heart. Intermittent aerobic exercise that elevated cardiac miR-101a expression plays an important role in the regulation of synchronous development of myocardial collagen hyperplasia and of myocardial fibers hypertrophy.8Intermittent aerobic exercise can significantly reduce myocardial local protein content of c-Fos/TGF-β1in MI rats and degrade myocardial fibrosis.9MI significantly reduced expression of miR-101a in rat myocardium and intermittent aerobic exercise can significantly elevate expression of miR-101a in myocardial local of MI rat and c-Fos/TGF-β1signaling pathway plays a role in degrading myoeardial fibrosis of the MI rats.Conclusion:1Intermittent aerobic exercise can reduce myocardial interstitial collagen deposition of the MI rats and improve cardiac function significantly.2Intermittent aerobic exercise can significantly elevate expression of miR-29a in the MI rat myocardium, and reduce the protein expression of TGF-β1/Smad2/3pathway.3Intermittent aerobic exercise can significantly elevate expression of miR-101a in the MI rat myocardium, and reduce the protein expression of c-Fos/TGF-β1pathway.The molecular mechanisms that intermittent aerobic exercise reduced infarct size and improved cardiac function effectively are related with increased expression of miR-101a/miR-29a and inhibition of its action sites and TGF-β1/Smad2/3and c-Fos/TGF-β1signaling pathways.
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