Combined treatment with anisodamine and neostigmine inhibits joint inflammation in collagen-induced arthritis mice

摘要

Rheumatoid arthritis (RA) is a complicated and treatment refractory autoimmune disease that is characterized by a chronic inflammatory infiltration of immune cells [1]. The central nervous system plays an important role in limiting inflammatory responses via an inflammatory reflex of the vagus nerve termed as "the cho-linergic antiinflammatory pathway" [2]. Acetylcholine, the principal neurotransmitter of the vagus nerve, interacts with alpha7 nicotinic acetylcholine receptor (alpha7nAChR) expressed on macro-phages and other cells and could inhibit the production of proin-flammatory cytokines such as TNFalpha, interleukin (IL)-1beta, and IL-6. Decreased level of vagus nerve activity is correlated with increased serum concentration of late-phase inflammation cytokine high-mobility group box chromosomal protein 1 in patients with RA. Stimulation of nicotinic acetylcholine receptors attenuates collagen-induced arthritis (CIA) in mice. Lack of alpha7nAChR aggravates the development of CIA [3].