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 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.
An ZHANGJun-ling CAOBo YANGJing-hong CHENZeng-tie ZHANGSi-yuan LIQiang FUClare E. HUGNESBruce CATERSON
