Objective To explore the effects of aerobic exercise training on the circulating miRNAs and their roles in cardio‐vascular adaption induced by aerobic exercise training .Methods Ten freshmen were enrolled .All subjects performed an 8 weeks swimming training .VO2 max and cardiovascular function were measured in acute exhaustive before and after the aerobic endurance training .The key circulating miRNs (miR‐133a ,miR‐21 ,miR‐146a ,miR‐199a ,miR‐15a and miR‐222) were measured at rest and im‐mediately following acute exhaustive exercise in competitive male freshmen before and after the aerobic training .Results Distinct patterns of c‐miRNA response to exercise were observed and adhere to 4 major profiles :after aerobic exercise training ,the levels of miR‐146a ,miR‐222 ,miR‐21 ,miR‐15a and miR‐199a at rest were significant higer than before training (P<0 .05) .The levels of miR‐146a and miR‐222 were up‐regulated by acute exercise before and after aerobic exercise training (P<0 .05) .Before the aerobic train‐ing ,acute exhaustive exercise increased miR‐21 and miR‐15a significantly(P<0 .05) ,however ,there was no difference between the miR‐21 and miR‐15a levels in acute exhaustive exercise and resting state after aerobic exercise training (P>0 .05) .There was no difference in the level of miR‐133a between resting state and acute exhaustive exercise before and after training (P>0 .05) .Further linear correlation analysis showed that the miR‐146a expression in plasma was significantly positively correlated with VO 2 max level (r=0 .842 ,P<0 .01) ,the change of miR‐222 expression in plasma before and after training was significantly positively correlated with EF (r=0 .920 ,P<0 .01) .Conclusion MiRNAs can be used as a marker to reflect the effect of training ,miR‐146a and miR‐222 play a role in physiological regulation of the cardiovascular function of aerobic exercise training in the body .

OBJECTIVE: To detect the effect of p38 mitogen activated protein kinase (p38MAPK) and cyclooxygenase-2 (COX-2) on the expression of mucin5AC (MUC5AC) in human nasal mucosa induced by histamine in vitro, and to investigate the pathogenesis of mucus hypersecretion in allergic rhinitis (AR). METHOD: Western blot was performed to detect the protein expressions of p38MAPK, COX-2 and MUC5AC in nasal mucosa induced by histamine or blocked by selective inhibitors of p38MAPK and COX-2 of different concentration gradient. RESULT: Weak expressions of p38MAPK. COX-2 and MUC5AC were detected in normal nasal mucosa in vitro. The protein expressions of p38MAPK. COX-2 and MUC5AC increased in nasal mucosa induced by histamine in a dose-dependent manner. The histamine induced protein expressions of COX-2 and MUC5AC were dose-dependently attenuated by selective inhibitor of COX-2, namely NS-398. No apparent influence of NS-398 on the expression of p38MAPK was observed. The histamine induced protein expressions of p38MAPK, C()X-2 and MUCbAC dose-dependently decreased after nasal mucosa was treated by selective inhibitor of p38MAPK, namely SB203580. And no significant change of MUC5AC protein expression induced by NS-398 or SB203580 was observed. CONCLUSION Our findings indicated that the histamine-induced increased expression of MUC5AC by activated p38MAPK/COX-2 may be a possible pathogenesis of mucus hypersecretion in AR.
Adult ; Female ; Humans ; Male ; Middle Aged ; Mucin 5AC ; metabolism ; Nasal Mucosa ; metabolism ; Rhinitis, Allergic, Perennial ; metabolism ; Signal Transduction ; p38 Mitogen-Activated Protein Kinases ; metabolism