Abstract

Panax notoginseng saponins are often used to treat a frequently of inflammatory diseases, but the underlying mechanisms of their effects on human osteoarthritis are limited. An osteoarthritis model was established by interleukin-1 beta treatment of chondrocytes for experiments. During the experiment, cell activity was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyl tetrazolium bromide method. The enzymelinked immunosorbent assay was applied to measure tumour necrosis factor alpha and interleukin-6 level, malondialdehyde content, superoxide dismutase activity, glutathione peroxidase activity in each group. Toll-like receptor 4 and myeloid differentiation factor 88 protein expression level was measured using Western blot. In this study, compared to the control group, the cell viability and the activity of superoxide dismutase and glutathione peroxidase in interleukin-1 beta group were notably reduced, while the content of malondialdehyde, interleukin-6 and tumour necrosis factor alpha, as well as the protein expression of tolllike receptor 4 and myeloid differentiation factor 88 were sharply increased. Compared with interleukin-1 beta group, cell viability, superoxide dismutase activity, glutathione peroxidase activity, malondialdehyde content were higher, whereas interleukin-6 and tumour necrosis factor alpha content and toll-like receptor 4 and myeloid differentiation factor 88 expression were lower in interleukin-1 beta+Panax notoginseng saponin groups. Moreover, relative to interleukin-1 beta+Panax notoginseng saponin-H+vector group, tolllike receptor 4 level and malondialdehyde, interleukin-6 and tumour necrosis factor alpha content were significantly increased, while cell activity, superoxide dismutase activity, glutathione peroxidase activity were considerably lowered in interleukin-1 beta+Panax notoginseng saponin H+toll-like receptor 4 group. Panax notoginseng saponins promoted interleukin-1 beta-stimulated osteoarthritis chondrocyte proliferation and inhibited cell oxidative damage and inflammatory response by modulating the toll-like receptor 4/myeloid differentiation factor 88 axis.