Ketorolac tromethamine represses senescence in aging articular chondrocytes

Biosci Biotechnol Biochem. 2022 Apr 11:zbac047. doi: 10.1093/bbb/zbac047. Online ahead of print.ABSTRACTThe present study aims to explore the potential function of ketorolac tromethamine in treating osteoarthritis (OA) by examining its effects on interleukin-1β (IL-1β)-triggered cellular senescence in chondrocytes. More β-galactosidase (SA-β-Gal) positively stained cells, promoted cell fraction in the G0/G1 phase, increased release of matrix metalloproteinase (MMP)-3 and MMP-13, and upregulated cellular senescence-related genes (p21 and p53) were observed in IL-1β-challenged HC-A cells, all of which were significantly reversed by 25 and 50 mg/mL ketorolac tromethamine. Furthermore, the upregulated cyclooxygenase-2 (COX-2) and elevated release of prostaglandin E2 (PGE2) in IL-1β- challenged HC-A cells were dramatically repressed by ketorolac tromethamine. Lastly, the inhibitory effects of ketorolac tromethamine on the activation of β-galactosidase and the upregulation of p21 and p53 were greatly abolished by the overexpression of COX-2. Collectively, ketorolac tromethamine repressed cellular senescence in aging articular chondrocytes by inhibiting COX-2.PMID:35404445 | DOI:10.1093/bbb/zbac047
Source: Bioscience, Biotechnology, and Biochemistry - Category: Biochemistry Authors: Source Type: research