Objective： To investigate the effects of mycotoxin moniliformin （MON） on the metabolism of aggrecan and type 11 collagen in human chondrocytes in vitro and the relationship between MON and Kashin-Beck disease （KBD...Objective： To investigate the effects of mycotoxin moniliformin （MON） on the metabolism of aggrecan and type 11 collagen in human chondrocytes in vitro and the relationship between MON and Kashin-Beck disease （KBD）. Methods： Human chondrocytes were isolated and cultured on bone matrix gelatin to form an artificial cartilage model in vitro with or without MON toxin. Cell viability was determined by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide （MTT） assay. The expression of aggrecan and type II collagen in the cartilage was determined using immunocytochemical staining. Results： MON toxin inhibited chondrocyte viability in dose-dependent and time-dependent manners. MON reduced aggrecan and type Ⅱ collagen syntheses in the tissue-engineered cartilage. MON also increased the expression of matrix metalloproteinase-1 （MMP-1）, MMP-13, BC4 epitopes, and CD44 in cartilages. However, the expression of 3B3（-） epitopes in cartilages was inhibited by MON. Selenium partially alleviated the damage of aggrecan induced by MON toxin. Conclusion： MON toxin promoted the catabolism of aggrecan and type II collagen in human chondrocytes.展开更多
基金Project supported by the National Natural Science Foundation of China (Nos.30872187,30471499,and 30170831)the Ministry of Education of China (No.Key 03152)the Science Foundation of Shaanxi Province of China (No.2004KW-20)
文摘Objective： To investigate the effects of mycotoxin moniliformin （MON） on the metabolism of aggrecan and type 11 collagen in human chondrocytes in vitro and the relationship between MON and Kashin-Beck disease （KBD）. Methods： Human chondrocytes were isolated and cultured on bone matrix gelatin to form an artificial cartilage model in vitro with or without MON toxin. Cell viability was determined by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide （MTT） assay. The expression of aggrecan and type II collagen in the cartilage was determined using immunocytochemical staining. Results： MON toxin inhibited chondrocyte viability in dose-dependent and time-dependent manners. MON reduced aggrecan and type Ⅱ collagen syntheses in the tissue-engineered cartilage. MON also increased the expression of matrix metalloproteinase-1 （MMP-1）, MMP-13, BC4 epitopes, and CD44 in cartilages. However, the expression of 3B3（-） epitopes in cartilages was inhibited by MON. Selenium partially alleviated the damage of aggrecan induced by MON toxin. Conclusion： MON toxin promoted the catabolism of aggrecan and type II collagen in human chondrocytes.
