Apocynin prevents cigarette smoking-induced loss of skeletal muscle mass and function in mice by preserving proteostatic signalling.

ABSTRACT:

Background and purpose

Skeletal muscle dysfunction is a major comorbidity of chronic obstructive pulmonary disease (COPD). This type of muscle dysfunction may be a direct consequence of oxidative insults evoked by cigarette smoke (CS) exposure. The present study examined the effects of a potent Nox inhibitor and reactive oxygen species (ROS) scavenger, apocynin, on CS-induced muscle dysfunction.

Experimental approach

Male BALB/c mice were exposed to either room air (sham) or CS generated from nine cigarettes per day, 5 days a week for 8 weeks, with or without the coadministration of apocynin (5 mg·kg^-1 , i.p.). C2C12 myotubes exposed to either hydrogen peroxide (H₂ O₂ ) or water-soluble cigarette smoke extract (CSE) with or without apocynin (

SUBMITTER: Chan SMH 

PROVIDER: S-EPMC8362135 | biostudies-literature | 2021 Aug

REPOSITORIES: biostudies-literature