Open AccessNomilin targets the Keap1‐Nrf2 signalling and ameliorates the development of osteoarthritis
Author(s) -
Xue XingHe,
Xue JiXin,
Hu Wei,
Shi FangLing,
Yang Yang
Publication year - 2020
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.15484
Subject(s) - osteoarthritis , inflammation , in vivo , keap1 , cartilage , cancer research , in vitro , chemistry , medicine , microbiology and biotechnology , immunology , biology , biochemistry , gene , pathology , anatomy , alternative medicine , transcription factor
Osteoarthritis (OA) is a long‐term and inflammatory disorder featured by cartilage erosion. Here, we describe nomilin (NOM), a triterpenoid with inflammation modulatory properties in variety of disorders. In this study, we demonstrated the latent mechanism of NOM in alleviating the progress of OA both in vitro and in vivo studies. The results showed that NOM pre‐treatment suppressed the IL‐1β–induced over‐regulation of pro‐inflammation factors, such as NO, IL‐6, PGE 2 , iNOS, TNF‐α and COX‐2. Moreover, NOM also down‐regulates the degradation of ECM induced by IL‐1β. Mechanistically, the NOM suppressed NF‐κB signalling via disassociation of Keap1‐Nrf2 in chondrocytes. Furthermore, NOM delays the disease progression in the mouse OA model. To sum up, this research indicated NOM possessed a new potential therapeutic option in osteoarthritis.