AIM: To investigate the effect of Nivalenol(NIV) and Selenium(Se) on the levels of IL-1beta and TNF-alpha in the cultured chondrocytes. METHODS: Human chondrocytes cultured in vitro were treated with or without NIV and Se. The morphology of chondrocytes was observed by optic microscope. The DNA content was determined by UV Spectrophotometry. The levels of IL-1beta and TNF-alpha in cultured medium were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: Hematoxylin & eosin staining indicated there was cell necrosis in the cartilage reconstructed in vitro from both NIV group and NIV+Se group. Compared with the group of NIV toxin, the damage of chondrocytes was less severe when Se was added. NIV could inhibit chondrocyte DNA synthesis. The content of DNA with NIV was lowest than that in other groups. The levels of IL-1beta and TNF-alpha with NIV were significantly higher than control group (P<0.05). After Se was added, the levels did not change significantly compared with the groups without Se. CONCLUSION: NIV toxin could superinduce IL-1beta and TNF-alpha secretion in chondrocytes, which may be the key mechanism of chondrocyte injury by NIV. Se can partially alleviate the effects of NIV on chondrocytes cultured in vitro.
AIM: To investigate the effect of Nivalenol(NIV) and Selenium(Se) on the levels of IL-1beta and TNF-alpha in the cultured chondrocytes. METHODS:Human chondrocytes cultured in vitro were treated with or without NIV and Se. The morphology of chondrocytes was observed by optic microscope. The DNA content was determined by UV Spectrophotometry. The levels of IL-1beta and TNF-alpha in cultured medium were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS:Hematoxylin & eosin staining indicated there was cell necrosis in the cartilage reconstructed in vitro from both NIV group and NIV+Se group. Compared with the group of NIV toxin, the damage of chondrocytes was less severe when Se was added. NIV could inhibit chondrocyte DNA synthesis. The content of DNA with NIV was lowest than that in other groups. The levels of IL-1beta and TNF-alpha with NIV were significantly higher than control group (P<0.05). After Se was added, the levels did not change significantly compared with the groups without Se. CONCLUSION: NIV toxin could superinduce IL-1beta and TNF-alpha secretion in chondrocytes, which may be the key mechanism of chondrocyte injury by NIV. Se can partially alleviate the effects of NIV on chondrocytes cultured in vitro.