Nicotinic acetylcholine receptor activation reduces skeletal muscle inflammation of mdx mice.

Abstract

Mdx mice develop an inflammatory myopathy characterized at different ages by myonecrosis with scattered inflammatory infiltrates followed by muscular regeneration and later persistent fibrosis. This work aimed to verify the putative anti-inflammatory role of nicotinic acetylcholine receptor (nAChR) in the mdx muscular lesion. Mitigation of myonecrosis and decreased TNFα production were accompanied by increased numbers of F4/80 macrophages expressing nAChRα7. In vivo treatment with nicotine attenuated muscular inflammation characterized by reduced metalloprotease MMP-9 activity, TNFα and NFkB content and increased muscular regeneration. Our data indicate that nAChR activation influences local inflammatory responses in the muscular lesion of mdx mice.