Objective:To investigate the effects of T-2 toxin on expressions of Fas,p53,Bcl-xL,Bcl-2,Bax and caspase-3 on human chondrocytes.Methods:Human chondrocytes were treated with T-2 toxin(1～20 ng/ml)for 5 d.Fas,p53 and other apoptosis-related proteins such as Bax,Bcl-2,Bcl-xL,caspase-3 were determined by Western blot analysis and their mRNA expressions were determined by reverse transcriptase-polymerase chain reaction(RT-PCR).Results:Increases in Fas,p53 and the pro-apoptotic factor Bax protein and mRNA expressions and a decrease of the anti-apoptotic factor Bcl-xL were observed in a dose-dependent manner after exposures to 1～20 ng/ml T-2 toxin,while the expression of the anti-apoptotic factor Bcl-2 was unchanged.Meanwhile,T-2 toxin could also up-regulate the expressions of both pro-caspase-3 and caspase-3 in a dose-dependent manner.Conclusion:These data suggest a possible underlying molecular mechanism for T-2 toxin to induce the apoptosis sig- naling pathway in human chondrocytes by regulation of apoptosis-related proteins.
Jing-hong CHEN Jun-ling CAO Yong-lie CHU Zhi-lun WANG Zhan-tian YANG Hong-lin WANG
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.
An ZHANGJun-ling CAOBo YANGJing-hong CHENZeng-tie ZHANGSi-yuan LIQiang FUClare E. HUGNESBruce CATERSON
