Activation of a7 Nicotinic Acetylcholine Receptors Prevents Monosodium Iodoacetate-Induced Osteoarthritis in Rats | Zendy

Yuan Liu | Zendy; Dongying Wu | Zendy; Fanglong Song | Zendy; Chenlei Zhu | Zendy; Yujian Hui | Zendy; Qingcheng Zhu | Zendy; Jie Wu | Zendy; Weimin Fan | Zendy; Jun Hu | Zendy

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Activation of a7 Nicotinic Acetylcholine Receptors Prevents Monosodium Iodoacetate-Induced Osteoarthritis in Rats

Author(s) -

Yuan Liu,

Dongying Wu,

Fanglong Song,

Chenlei Zhu,

Yujian Hui,

Qingcheng Zhu,

Jie Wu,

Weimin Fan,

Jun Hu

Publication year - 2015

Publication title -

cellular physiology and biochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.486

H-Index - 87

eISSN - 1421-9778

pISSN - 1015-8987

DOI - 10.1159/000369724

Subject(s) - methyllycaconitine , nicotine , mapk/erk pathway , kinase , chemistry , pharmacology , nicotinic agonist , p38 mitogen activated protein kinases , cholinergic , acetylcholine receptor , protein kinase a , nicotinic antagonist , receptor , nicotinic acetylcholine receptor , microbiology and biotechnology , endocrinology , medicine , biology , biochemistry

Although some evidence suggests that the prevalence of osteoarthritis (OA) is lower in smokers compared to nonsmokers, the mechanisms of nicotine-induced protection remain unclear. Stimulation of the α7 nicotinic acetylcholine receptor (α7-nAChR) appears to be a critical mechanism underlying the anti-inflammatory potential of cholinergic agonists in immune cells. The inhibition of secreted inflammatory molecules and the subsequent inflammatory processes have been proposed as a novel strategy for the treatment of OA. The objective of the present study was to determine whether nicotine-induced protection in a monosodium iodoacetate (MIA) rat model of OA occurs via α7-nAChR-mediated inhibition of chondrocytes.

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