Coptisine Prevented IL-β-Induced Expression of Inflammatory Mediators in Chondrocytes.
Interleukin 1β (IL-1β) is a pleiotropic pro-inflammatory cytokine that plays a critical role in the development of osteoarthritis (OA). Coptisine is an isoquinoline alkaloid extracted from Coptidis rhizome and has been reported to possess anti-inflammatory activity. However, the anti-inflammatory effects of coptisine on interleukin-1 beta (IL-1β)-stimulated chondrocytes have not been reported. Therefore, the aim of this study was to investigate the effects of coptisine on IL-1β-induced inflammation in human articular chondrocytes. Our results showed that coptisine greatly inhibited the production of nitric oxide (NO) and prostaglandin E2 (PGE2), as well as suppressed the expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) in human OA chondrocytes induced by IL-1β. It also inhibited the expression of matrix metalloproteinase-3 (MMP-3) and MMP-13 in IL-1β-stimulated human OA chondrocytes. Furthermore, coptisine significantly inhibited the IL-1β-induced NF-kB activation in human OA chondrocytes. Taken together, these data suggest that coptisine inhibits the IL-1β-induced inflammatory response by suppressing the NF-kB signaling pathway. Thus, coptisine may be a potential agent in the treatment of OA.
Department of Emergency, The Affiliated Hospital of Southwest Medical University, No. 25 Taiping Road, Luzhou, 646000, China. zhoukailuz@163.com.
Kai
K
Zhou
Department of Emergency, The Affiliated Hospital of Southwest Medical University, No. 25 Taiping Road, Luzhou, 646000, China.
Li
L
Hu
Department of Emergency, The Affiliated Hospital of Southwest Medical University, No. 25 Taiping Road, Luzhou, 646000, China.
Wenjun
W
Liao
Department of Emergency, The Affiliated Hospital of Southwest Medical University, No. 25 Taiping Road, Luzhou, 646000, China.
Defeng
D
Yin
Basic Medical College of Xinjiang Medical University, No. 393 Xinyi Road, Urumqi, 830054, China. ruifang_phd@163.com.
Feng
F
Rui
D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D001599:Berberine / Q000031:analogs & derivatives* / Q000494:pharmacology; D002478:Cells, Cultured; D019902:Chondrocytes / Q000378:metabolism* / Q000473:pathology; D051546:Cyclooxygenase 2 / Q000187:drug effects; D006801:Humans; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors* / Q000378:metabolism; D053583:Interleukin-1beta / Q000502:physiology*; D016328:NF-kappa B / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000037:antagonists & inhibitors
D000893:Anti-Inflammatory Agents; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D016328:NF-kappa B; C034384:coptisine; D001599:Berberine; C496319:NOS2 protein, human; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2
chondrocyte; coptisine; interleukin-1 beta (IL-1β); osteoarthritis (OA)