Abstract

Using both cellular and animal models, this research assessed emodin effect on human chondrocytes as well as its underlying anti-inflammatory mechanisms. The results demonstrated that emodin had no significant impact on cell viability in normal chondrocytes, but exhibited a dose-dependent protective effect on lipopolysaccharides-induced inflammatory chondrocytes and inhibition of cell apoptosis. Moreover, emodin was found to reduce the levels of inflammatory cytokines induced by lipopolysaccharides. Mechanistically, emodin decreased the levels of reactive oxygen species in lipopolysaccharides-treated TC28a2 human chondrocyte cells and hampered the stimulation of the high mobility group box-1/toll-like receptor 4/nuclear factor kappa B signaling pathway. In a knee osteoarthritis rat model, emodin improved the morphology of cartilage tissue, suppressed cell apoptosis, and restrained the high mobility group box-1/toll-like receptor 4/nuclear factor kappa B signaling pathway and reactive oxygen species accumulation. In summary, emodin exhibited an anti-inflammatory effect, improving cell survival, suppressing apoptosis in chondrocytes, as well as reducing the levels of inflammatory cytokines, which might be achieved by modulating the high mobility group box-1/toll-like receptor 4/nuclear factor kappa B signaling pathway and reactive oxygen species levels. These results indicate that emodin seems to have therapeutic value in the treatment of knee osteoarthritis.