Influence Of Uric Acid On Cell Viability And Expression Of Inflammatory Factors Of Chondrocytes

Objective: To detect the cell viability and the expression of interleukin-1 beta(IL-1?), tumor necrosis factor-alpha(TNF-?) of chondrocytes which were treated with different concentrations of uric acid(UA) for different times in vitro, to explore the influence of different concentration of uric acid on the cartilage.Methods: The articular cartilage cells of rats were cultured in vitro, and then the cells were treated with uric acid solution of the concentrations of 0, 4, 8, 10, 16, 32 mg/d L for 24?48 hours respectively. The cell viability of rat articular cartilage was assessed by MTT. The levels of IL-1? and TNF-? in cell supernatant fluid were measured by ELISA.Results: With differente concentrations at the same time: The cell viability of 4 mg/d L UA group was lower than that in the control group(0 mg/d L), having no difference(P>0.05); The cell viability of 8, 10, 16, 32 mg/d L UA groups was significantly lower than that in the control group and decreased with the increase of the concentration of uric acid(P<0.05). The levers of IL-1? and TNF-? in 4, 8, 10 mg/d L UA groups were higher than that in the control group(P<0.05) and increased with the increase of the concentration of uric acid. The levers of IL-1? and TNF-? in 10, 16, 32 mg/d L UA groups were higher than that in the control group(P < 0.05) but decreased with the increase of the concentration of uric acid. With the same concentrations at differente times: 48 h comparied with 24 h, the cell viability of cartilage cells was lower(P>0.05) and the expression of IL-1? and TNF-? of cartilage cells were higher(P<0.05).Conclusions: Uric acid inhibits cell viability of cartilage cells; at the same time, it significantly promotes the expression of IL-1? and TNF-? in the range of 4-10 mg/d L. However, after more than 10 mg/d L of uric acid, this effect is gradually weakened with the serious decline of cell viability. This may be the important factors that uric acid involves in the cartilage damage, as well as the pathogenesis of osteoarthritis.