Muscle ring-finger protein (MuRF1) inhibitor and exercise training ameliorates functional and structural changes induced by cigarette smoke exposure in an experimental model of chronic obstructive pulmonary disease.

Le résumé fourni par la source

A decrease of respiratory function, sarcopenia, and weight loss characterizes chronic obstructive pulmonary disease (COPD). Studies show that exercise training can attenuate COPD development in animal models. The positive regulation of MuRF1 is fundamental in regulating muscle mass and associated with exercise could benefit patients with COPD. This study aimed to investigate MuRF1 inhibition combined with exercise training in a COPD model induced by cigarette smoke exposure. Mice were exposed to CS for 3 months (2x per day, 5 days per week) and received MyoMed 205 (MuRF1 inhibitor) in their daily diet. Randomized animals were submitted to an exercise training protocol (1x per day, 5 days per week for 90 days). Five experimental groups: Con: vivarium with filtered air; CS: exposed to cigarette smoke; CS+Exe: exposed to cigarette smoke and exercise training; CS+205: exposed to cigarette smoke and MyoMed 205; CS+Exe+205:exposed to cigarette smoke, exercise, and MyoMed 205. Physical capacity was assessed by maximal treadmill effort. Respiratory mechanics were evaluated by tissue elastance (Htis). Results: Table 1. Alveolar enlargement was assessed by the mean linear intercept (Lm). MuRF1 inhibitor and exercise training reversed structural and functional changes caused by CS exposure in this COPD model. erj;66/suppl_69/OA1286/F1 F1 F1

Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.