Isoquercetin Ameliorates Osteoarthritis via Nrf2/NFκB Axis: An In Vitro and In Vivo Study

Author:

Yu He1,Lou Junsheng2,Ni Libin1,Yan Minwei1,Zhu Kewu3,Mao Su1,Zhu Jungao1ORCID

Affiliation:

1. Department of Orthopaedics Zhejiang Hospital Zhejiang Hangzhou China

2. Department of Orthopedic Surgery, The First Affiliated Hospital Zhejiang University School of Medicine Zhejiang Hangzhou China

3. Center for Drug Delivery System Research, School of Medicine Shaoxing University Shaoxing Zhejiang China

Abstract

ABSTRACTOsteoarthritis (OA) is a progressive joint disease characterized by extracellular matrix (ECM) degradation and inflammation, which is involved with pathological microenvironmental alterations induced by damaged chondrocytes. However, current therapies are not effective in alleviating the progression of OA. Isoquercetin is a natural flavonoid glycoside compound that has various pharmacological effects including anticancer, anti‐diabetes and blood lipid regulation. Previous evidence suggests that isoquercetin has anti‐inflammatory properties in various diseases, but its effect on OA has not been investigated yet. In this study, through western bolt, qRT‐PCR and ELISA, it was found that isoquercetin could reduce the increase of ADAMTS5, MMP13, COX‐2, iNOS and IL‐6 induced by IL‐1β, suggesting that isoquercetin could inhibit the inflammation and ECM degradation of chondrocytes. Through nuclear‐plasma separation technique, western blot and immunocytochemistry, it can be found that Nrf2 and NF‐κB pathways are activated in this process, and isoquercetin may rely on this process to play its protective role. In vivo, the results of X‐ray and SO staining show that intra‐articular injection of isoquercetin reduces the degradation of cartilage in the mouse OA model. In conclusion, the present work suggests that isoquercetin may benefit chondrocytes by regulating the Nrf2/NF‐κB signaling axis, which supports isoquercetin as a potential drug for the treatment of OA.

Publisher

Wiley

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