Anthocyanins and metabolites from purple rice inhibit IL-1β-induced matrix metalloproteinases expression in human articular chondrocytes through the NF-κB and ERK/MAPK pathway

• Main Authors: Tunchanok Wongwichai, Pimpisa Teeyakasem, Dumnoensun Pruksakorn, Prachya Kongtawelert, Peraphan Pothacharoen
• Format: Journal
• Published: 2019
• Subjects: Pharmacology, Toxicology and Pharmaceutics
• Online Access: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85061775281&origin=inward; http://cmuir.cmu.ac.th/jspui/handle/6653943832/63753
• Institution: Chiang Mai University

© 2019 The Authors Osteoarthritis (OA) is a common degenerative joint disease, which is closely related to cartilage degradation. Anthocyanins, a natural flavonoid pigments, exhibit strong antioxidant and anti-inflammatory properties. However, the effect of anthocyanin on inflammatory response in OA has not been investigated. Our results showed that cyanidin-3-O-glucoside (C3G) and peonidin-3-O-glucoside (P3G), the main anthocyanins found in three Thai purple rice cultivars, attenuated the inhibition of porcine cartilage degradation in an experimental model. The effects of three Thai purple rice extracts were related to their high concentration of anthocyanins. Moreover, protocatechuic acid (PA), the main metabolite of anthocyanin, has chondroprotective potential by reducing glycosaminoglycans and collagen breakdown in IL-1β/OSM-induced porcine cartilage explants in long-term condition. The induction of matrix metalloproteinases (MMPs) caused by IL-1β-stimulated human chondrocytes was also attenuated by C3G, P3G, and their metabolites. Furthermore, C3G, P3G, and their metabolites pretreatment significantly inhibited IκBα degradation, the level of p-p65, and ERK/MAPK pathway. Additionally, PA pretreatment enhanced the phosphorylation of JNK in IL-1β-stimulated human chondrocytes. These findings indicated that anthocyanin in Thai purple rice exhibited anti-inflammatory effects in IL-1β-stimulated human chondrocytes by inhibiting NF-κB and ERK/MAPK signaling pathway.