Micheliolide Inhibits Interleukin-1 ss-Induced Inflammation by Downregulating MAPK in Chondrocytes

Background: Micheliolide (MCL) has ameliorating effects on tissue inflammation, but its potential therapeutic effect on osteoarthritis (OA) is unknown. The study aims to explore the pharmacological action and mechanism of MCL in the treatment of OA. Methods: Two models of OA were established and treated with MCL. Chondrocyte activity was evaluated by cell counting kit (CCK)-8 assay, while prostaglandin E2 (PGE2), nitric oxide (NO), and interleukin-1 ss (IL-1 ss) levels were measured using commercial kits. Mitogen activated protein kinase (MAPK) pathway-related proteins were evaluated by Western blotting, while key enzymes in cartilage degradation were analyzed by real-time quantitative polymerase chain reaction. Cartilage injury in OA mice was assessed by Saffranine O green staining, whereas pathological injury of brain, lung, kidney, and heart was determined by hematoxylin-eosin staining. Results: MCL suppressed the production of IL-1 ss-induced PGE2 and NO, cyclooxygenase 2, and inducible nitric oxide synthase in mouse chondrocytes. MCL also inhibited IL-1 ss-induced disintegrin and metalloproteinase with thrombospondin motif 4/5 mRNA and matrix metalloproteinases. MAPK pathway was inhibited by MCL. MCL effectively inhibited OA in mice. Conclusions: MCL inhibits IL-1 ss-stimulated chondrocyte inflammation by blocking the MAPK pathway. The application of MCL in the treatment of OA provides new data support.

Automated summary

This study aimed to investigate the pharmacological action and mechanism of Micheliolide (MCL) in the treatment of osteoarthritis (OA). The results showed that MCL can inhibit IL-1β-induced chondrocyte inflammation by blocking the MAPK pathway. These findings provide new data support for the application of MCL in the treatment of OA.