Puerarin suppresses inflammation and ECM degradation through Nrf2/HO-1 axis in chondrocytes and alleviates pain symptom in osteoarthritic mice

Osteoarthritis (OA) is the most common degenerative joint disorder with no effective drugs. Puerarin is a dietary supplement that has wide-ranging pharmacological effects. This study aimed to investigate the effects of Puerarin on OA. The effects of Puerarin on apoptosis, extracellular matrix (ECM)...

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Veröffentlicht in:Food & function 2021-03, Vol.12 (5), p.275-289
Hauptverfasser: Chen, Ximiao, Huang, Chongan, Sun, Haiqiu, Hong, Haofeng, Jin, Jie, Bei, Chaoyong, Lu, Zhongqiu, Zhang, Xiaolei
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Sprache:eng
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Zusammenfassung:Osteoarthritis (OA) is the most common degenerative joint disorder with no effective drugs. Puerarin is a dietary supplement that has wide-ranging pharmacological effects. This study aimed to investigate the effects of Puerarin on OA. The effects of Puerarin on apoptosis, extracellular matrix (ECM) metabolism, and inflammation-related factors were assessed; also, the nuclear factor-κB (NF-κB) signaling pathway and Nrf2/HO-1 (nuclear factor (erythroid-derived 2)-like 2/heme oxygenase-1) axis were evaluated to elucidate the working mechanism of Puerarin. Mice were fed with Puerarin to evaluate the therapeutic effect of Puerarin on Osteoarthritis in vivo . The results showed that Puerarin suppressed inflammatory mediators and apoptosis induced by IL-1β treatment in chondrocytes, it may also suppress ECM degradation in IL-1β treated chondrocytes. The mechanism study revealed that Nrf2/HO-1 pathway is involved in Puerarin induced inhibition of NF-κB signaling pathway. Finally, in vivo study demonstrated that Puerarin could postpone the progression of OA in mice and relieve the symptoms of pain. In conclusion, Puerarin may potentially alleviate OA progression, and the mechanism may relate to the Nrf2/HO-1 pathway regulation. Puerarin suppresses the NF-κB signaling pathway by activating the Nrf2/HO-1 axis, thereby inhibiting IL-1β-induced inflammation and ECM degradation in Osteoarthritis.
ISSN:2042-6496
2042-650X
DOI:10.1039/d0fo03076g