Effects of moniliformin and selenium on human articular cartilage metabolism and their potential relationships to the pathogenesis of Kashin-Beck disease  

作　　者：An ZHANG Jun-ling CAO Bo YANG Jing-hong CHEN Zeng-tie ZHANG Si-yuan LI Qiang FU Clare E. HUGNES Bruce CATERSON 

机构地区：[1]Institute of Endemic Diseases, School of Medicine, Xi 'an Jiaotong University, Xi 'an 710061, China [2]Key Laboratory of Environment and Genes Related to Diseases of Ministry of Education, Xi 'an Jiaotong University, Xi 'an 710061, China [3]Key Laboratory of Microelement and Endemic Disease of Ministry of Health, Xi 'an Jiaotong University, Xi'an 710061, China [4]Laboratory of Connective Tissue Biology, School of Biosciences, Cardiff University, Cardiff CF10 3US, UK

出　　处：《Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)》2010年第3期200-208,共9页浙江大学学报（英文版）B辑（生物医学与生物技术）

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)

摘　　要：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.Objective:To investigate the effects of mycotoxin moniliformin (MON) on the metabolism of aggrecan and type II 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.

关 键 词：CHONDROCYTES MONILIFORMIN SELENIUM AGGRECAN Collagen Matrix metalloproteinases （MMPs） CD44 Kashin-Beck disease 

分 类 号：Q954.657[生物学—动物学] X503[环境科学与工程—环境工程]