Tormentic Acid Inhibits IL-1β-Induced Inflammatory Response in Human Osteoarthritic Chondrocytes.
The pro-inflammatory cytokine interleukin-1beta (IL-1β) plays critical roles in pathogenesis of osteoarthritis (OA). Tormentic acid (TA), a triterpene isolated from Rosa rugosa, has anti-inflammatory activity. However, the anti-inflammatory effect of TA on OA is still unclear. So, in the present study, we examined the effect of TA on IL-1β-induced inflammatory response in primary human OA chondrocytes. Our results demonstrated that TA significantly decreased the IL-1β-stimulated expression of matrix metalloproteinase-3 (MMP-3) and MMP-13. It also inhibited the IL-1β-induced expression of inducible nitric oxide (NO) synthase (iNOS) and cyclooxygenase-2 (COX-2), as well as the production of NO and prostaglandin E2 (PGE2) in human OA chondrocytes. Furthermore, TA greatly inhibited the IL-1β-induced NF-κB activation. In conclusion, this study is the first to demonstrate the anti-inflammatory activity of TA in human OA chondrocytes. TA significantly inhibits the IL-1β-induced inflammatory response by suppressing the NF-κB signaling pathway. Thus, TA may be a potential agent in the treatment of OA.
Department of Orthopedics, Tianjin Hospital, Tianjin, 300211, China.
Yang
Y
Yang
Department of Electromyography, Tianjin Hospital, Tianjin, 300211, China.
Yawei
Y
Wang
Department of Orthopedics, Tianjin Hospital, Tianjin, 300211, China.
Yumin
Y
Wang
Clinical laboratory, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, China.
Meng
M
Zhao
Department of Orthopedics, Tianjin Hospital, Tianjin, 300211, China.
Haobo
H
Jia
Department of Orthopedics, Tianjin Hospital, Tianjin, 300211, China. braveman1982@163.com.
Bing
B
Li
Arthritis Clinic & Research Center, Peking University People's Hospital, Peking University, Beijing, 100044, China. xingdan@bjmu.edu.cn.
Dan
D
Xing
D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D002478:Cells, Cultured; D019902:Chondrocytes / Q000187:drug effects; D006801:Humans; D007249:Inflammation / Q000139:chemically induced / Q000188:drug therapy*; D020382:Interleukin-18 / Q000494:pharmacology; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000378:metabolism; D010003:Osteoarthritis / Q000188:drug therapy / Q000473:pathology*; D015398:Signal Transduction / Q000187:drug effects; D014315:Triterpenes / Q000494:pharmacology*
D000893:Anti-Inflammatory Agents; D020382:Interleukin-18; D016328:NF-kappa B; D014315:Triterpenes; C007695:euscaphic acid
chondrocyte; interleukin-1beta (IL-1β); osteoarthritis (OA); tormentic acid (TA)