Glycyrrhizin, an HMGB1 inhibitor, Suppresses Interleukin-1β-Induced Inflammatory Responses in Chondrocytes from Patients with Osteoarthritis

Background. High mobility group box 1 (HMGB1) is increased in osteoarthritis (OA) tissue and chondrocytes stimulated with interleukin- 1 beta (IL-1 beta). Suppression of HMGBI expression is correlated with reduced inflammatory responses induced by IL-1 beta. This study aimed to investigate how inhibition of HMGB1 by glycyrrhizin might affect inflammatory responses and viability of OA patient-derived chondrocytes treated with IL-1 beta. Design. The amounts of HMGB1 in the cartilage tissue and synovial fluid in patients with OA were assessed by Western blot and enzyme-linked immunosorbent assay (ELISA). Chondrocytes were extracted from OA patients and maintained in culture. The impact of glycyrrhizin on IL-1 beta-induced cell toxicity and inflammatory mediators and cytokines, including prostaglandin E2 (PGE(2)), nitric oxide (NO), proinflammatory cytokines, and metalloproteases (MMPs), were assessed by ELISA, Western blot, quantitative real-time polymerase chain reaction, and the Griess reagent assay. Results. We confirmed that HMGB1 was significantly upregulated in specimens acquired from patients with OA. HMGB1 inhibition by glycyrrhizin improved cell viability of chondrocytes treated with IL-1 beta. Glycyrrhizin suppressed IL-1 beta-induced upregulation of HMGB1 and inflammatory mediators and cytokines, including PGE(2), NO, proinflammatory cytokines, and MMPs. Conclusion. Our results indicate that glycyrrhizin may be a potential therapy for OA patients and these promising findings warrant further study for clinical application.

Automated summary

The study found that HMGB1 levels were significantly increased in OA patients' cartilage tissue, and glycyrrhizin was shown to inhibit IL-1 beta-induced upregulation of HMGB1 and inflammatory mediators, improving chondrocyte viability. Glycyrrhizin may be a potential therapy for OA patients and further research is needed for clinical application.