Abstract

Chondrocyte dysfunction and apoptosis are the two critical features during the progression of osteoarthritis. Corilagin, a gallotannin, is isolated from Caesalpinia coriaria (Jacq.). It was reported to possess anti-inflammatory, anti-tumor and hepatoprotective activities. However, this study aims to investigate the role of corilagin in osteoarthritis and the potential mechanism of action. Primary rat chondrocytes were treated with interleukin-1 beta and various concentrations of corilagin. Terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling staining, reverse transcription quantitative polymerase chain reaction, Western blot and immunofluorescence staining evaluated apoptotic levels, catabolic metabolism and relative signaling pathways. Corilagin suppressed chondrocyte cell viability reduction, lactate dehydrogenase, and inflammatory cytokine release and apoptosis triggered by interleukin-1 beta. Corilagin inhibited the interleukin-1 beta induced reduction in extracellular matrix protein collagen II and collagen type II alpha-1 and aggrecan messenger ribonucleic acid expression. Corilagin also enhanced protein expression of collagen II, ADAM metallopeptidase with thrombospondin type 1 motif 5, and sirtuin 1 and attenuated the nuclear expression of nuclear factor kappa B p65 in interleukin-1 beta treated chondrocytes. Corilagin attenuates interleukin-1 beta induce inflammatory response, apoptosis and catabolism in rat chondrocytes, and the mechanism might be associated with the activation of the sirtuin 1 nuclear factor kappa B pathway. Our results speculate that corilagin could be a potential therapeutic agent in treating osteoarthritis.