Protective effect of glycyrrhizin on osteoarthritis cartilage degeneration and inflammation response in a rat model

This study was conducted to investigate the protective effects of glycyrrhizin on a rat model of osteoarthritis and elucidate the underlying mechanism. Rat osteoarthritis was established by using medial meniscectomy (MMx) and an anterior cruciate ligament transaction (ACLT). Glycyrrhizin (2, 4, and 10 mg/kg) was administered by intra-articular knee injection for 12 weeks. Incapacitance test was performed to determine mechanical hyperalgesia. Enzyme-linked immunosorbent assay (ELISA) was performed to measure cartilage degradation and inflammation-related markers. Quantitative reverse transcription PCR (RT-qPCR) and Western blot were performed to determine the mRNA and protein levels of genes, respectively. The results demonstrated that treatment with glycyrrhizin ameliorated mechanical hyperalgesia and bilateral joints oedema in a rat model of osteoarthritis. Treatment with 10 mg/kg glycyrrhizin also suppressed serum enzymes including matrix metalloproteinase (MMP)-1, MMP-3, prostaglandin E2, and C-telopeptide of type II collagen (CTX-II). In addition to inhibition of cartilage matrix catabolic related markers, treatment with glycyrrhizin also decreased the levels of interleukin (IL)-1 beta, IL-6, tumor necrosis factor (TNF)-alpha, and iNOS in serum and cartilage. The underlying mechanism study demonstrated that treatment with glycyrrhizin inhibited HMGB1 and the TLR4/NF-kappa B signaling pathway. In summary, treatment with glycyrrhizin ameliorated cartilage degeneration and inflammation in osteoarthritis rats by the regulation of HMGB1 and the TLR4/NF-kappa B signaling pathway.

Automated summary

The study demonstrated that treatment with glycyrrhizin alleviated mechanical hyperalgesia and joint edema in a rat model of osteoarthritis, as well as suppressed the release of enzymes and inflammatory markers. Additionally, glycyrrhizin treatment regulated cartilage degeneration and inflammation by inhibiting HMGB1 and the TLR4/NF-kappa B signaling pathway.