Echinocystic Acid Inhibits IL-1β-Induced COX-2 and iNOS Expression in Human Osteoarthritis Chondrocytes.
Echinocystic acid (EA), a pentacyclic triterpene isolated from the fruits of Gleditsia sinensis Lam, displays a range of pharmacological activities including anti-inflammatory and antioxidant effects. However, the effect of EA on IL-1β-stimulated osteoarthritis chondrocyte has not been reported. The purpose of this study was to assess the effects of EA on IL-1β-stimulated human osteoarthritis chondrocyte. Chondrocytes were stimulated with IL-1β in the absence or presence of EA. NO and PGE2 production were measured by Griess reagent and ELISA. The expression of COX-2, iNOS, nuclear factor-κB (NF-κB), inhibitory kappa B (IκBα), c-Jun N-terminal kinase (JNK), p38, and extracellular signal-regulated kinase (ERK) were detected by Western blot analysis. The results showed that EA suppressed IL-1β-induced collagenase-3 (MMP-13), NO, and PGE2 production in a dose-dependent manner. IL-1β up-regulated the expression of COX-2 and iNOS, and the increase was inhibited by EA. Furthermore, IL-1β-induced NF-κB and mitogen-activated protein kinase (MAPK) activation were inhibited by EA. In conclusion, EA effectively attenuated IL-1β-induced inflammatory response in osteoarthritis chondrocyte which suggesting that EA may be a potential agent in the treatment of osteoarthritis.
Department of Orthopedic Surgery, The Second Hospital of Harbin Medical University, Harbin, Heilongjiang Province, 150086, People's Republic of China.
Zhiqiang
Z
Ma
Department of Orthopedic Surgery, The Second Hospital of Harbin Medical University, Harbin, Heilongjiang Province, 150086, People's Republic of China.
Yanlong
Y
Wang
Children's Hospital of Harbin, Harbin, Heilongjiang Province, 150010, People's Republic of China.
Taikui
T
Piao
Department of Orthopedic Surgery, The Second Hospital of Harbin Medical University, Harbin, Heilongjiang Province, 150086, People's Republic of China. liujianyuls@163.com.
Jianyu
J
Liu
D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D000975:Antioxidants / Q000494:pharmacology*; D002358:Cartilage, Articular / Q000166:cytology; D002478:Cells, Cultured; D019902:Chondrocytes / Q000166:cytology / Q000378:metabolism*; D051546:Cyclooxygenase 2 / Q000096:biosynthesis*; D015232:Dinoprostone / Q000378:metabolism; D004789:Enzyme Activation / Q000187:drug effects; D048049:Extracellular Signal-Regulated MAP Kinases / Q000096:biosynthesis; D006801:Humans; D053583:Interleukin-1beta / Q000037:antagonists & inhibitors*; D048031:JNK Mitogen-Activated Protein Kinases / Q000096:biosynthesis; D053509:Matrix Metalloproteinase 13 / Q000378:metabolism; D008875:Middle Aged; D000072000:NF-KappaB Inhibitor alpha / Q000096:biosynthesis; D016328:NF-kappa B / Q000096:biosynthesis; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000096:biosynthesis*; D009828:Oleanolic Acid / Q000031:analogs & derivatives* / Q000494:pharmacology; D010003:Osteoarthritis / Q000188:drug therapy / Q000378:metabolism*; D048051:p38 Mitogen-Activated Protein Kinases / Q000096:biosynthesis
D000893:Anti-Inflammatory Agents; D000975:Antioxidants; C508585:IL1B protein, human; D053583:Interleukin-1beta; D016328:NF-kappa B; D000072000:NF-KappaB Inhibitor alpha; D009569:Nitric Oxide; D009828:Oleanolic Acid; C496319:NOS2 protein, human; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D048049:Extracellular Signal-Regulated MAP Kinases; D048031:JNK Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases; C507079:MMP13 protein, human; D053509:Matrix Metalloproteinase 13; D015232:Dinoprostone; C022999:echinocystic acid
IL-1β; NF-κB; echinocystic acid; osteoarthritis chondrocyte