ReferenceID 1187
Apocynin prevents cigarette smoking-induced loss of skeletal muscle mass and function in mice by preserving proteostatic signalling
Br J Pharmacol
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 cigar
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- Reference Id
- 1187
- Evidence Id
- 17777
- Core Evidence Id
- 17777
- Source Reference Id
- 2358
- Herb2 Reference Id
- HBREF003155
- Subject Paper Key
- HBIN016505_33817783
- Pubmed Id
- 33817783
- Doi
- 10.1111/bph.15482
- Paper Title
- Apocynin prevents cigarette smoking-induced loss of skeletal muscle mass and function in mice by preserving proteostatic signalling
- Paper 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 (500 nM) were used as an experimental model in vitro. KEY RESULTS: Eight weeks of CS exposure caused muscle dysfunction in mice, reflected by 10% loss of muscle mass and 54% loss of strength of tibialis anterior which were prevented by apocynin administration. In C2C12 myotubes, direct exposure to H2 O2 or CSE caused myofibre wasting, accompanied by ~50% loss of muscle-derived insulin-like growth factor (IGF)-1 and two-fold induction of Cybb, independent of cellular inflammation. Expression of myostatin and MAFbx, negative regulators of muscle mass, were up-regulated under H2 O2 but not CSE conditions. Apocynin treatment abolished CSE-induced Cybb expression, preserving muscle-derived IGF-1 expression and signalling pathway downstream of mammalian target of rapamycin (mTOR), thereby preventing myofibre wasting. CONCLUSION AND IMPLICATIONS: Targeted pharmacological inhibition of Nox-derived ROS may alleviate the lung and systemic manifestations in smokers with COPD.
- Journal
- Br J Pharmacol
- Publish Year
- 2021
- Experiment Subject
- mouse; c2c12 myotubes
- Experiment Type
- Animal Experiment
- Phenotype Related
- Lung And Systemic Manifestations; Myofibre Wasting; Skeletal Muscle Dysfunction; Chronic Obstructive Pulmonary Disease; Muscle Dysfunction
- Paper Title Cn
- Paper Title En
- Apocynin prevents cigarette smoking-induced loss of skeletal muscle mass and function in mice by preserving proteostatic signalling
- Bilingual Status
- semi_complete