Effects of Endurance Exercise of Different Intensity on TGF-β1/miR-21 Signaling Pathpay

Objective:To explore effects of different sustained intensive exercise on rat atrial hydroxyproline,and role of TGF-β1/miR-21 signaling pathway through establishing long-term exercise animal model,and provide experimental evidence for clarifiying the mechanism of exercise-induced atrial fibrillation.Methods:72SD rats were divided into control group(C),moderate intensity group(M)and high instensity group(H)with 24 animals in each group.M and H group were conditioned to run for 4,8,and 16 weeks,5days/weeks,1h/day.Rats were euthanized to obtain hearts within 24 hafter exercise.Right atrial were collected.cTnI was quantified by Elisa,hydroxyproline was measured by lkali hydrolysis methodwhich.TGF-β1and miR-21 gene expression were evaluted by real-time PCR.TGF-β1protein was quantified by Western Blot.Results:Compared with control and M group,rats serum cTnI increased at 8 weeks/12 weeks/16 weeks(P <0.01).While there was no significance between M group and C gourp.There was no significant difference in hydroxyproline at 8 weeks.Compared with C and M group,hydroxyproline content of H group showed significant increase at12 weeks and 16 weeks(P<0.01).No difference was oberserved between C group and M group.Hydroxyproline content of H group confirmed a gradual increase with training time,with significant increase from 8weeks to 16weeks(P<0.05).TGF-β1gene and protein expression of H group increased compared their control group at 8/12/16 weeks.But no difference was observed between C and M group.TGF-β1expression had a gradual decrease from 8to 16 weeks.Compared with their control group,miR-21 expressio of H group showed a significant increase(P<0.05).miR-21 of H group confirmed a gradual decrease with training time,with significant decrease from 8weeks to 16weeks(P<0.05).No significant difference was observed beteen C and M group.Conclusion:Long-term intensive exercise induced sustained myocardial damage,resulted in sustained collagen increase which induced myocardial fibrosis.This may be a substrate for exercise-induced atrial fibrillation.TGF-β1/miR-21 signaling pathway,upregulated by long-term intensive exercise,may involve in the pathology of intense exercise-induced myocardial damage and atrial fibrillation.