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Increased Chondrocyte Apoptosis in Kashin-Beck Disease and Rats Induced by T-2 Toxin and Selenium Deficiency

查看全文 作　　者：YANG Hao [1,2]Jie;ZHANG [1]Ying;WANG Zhi [1]Lun;XUE Sen [1]Hai;LI Si [1]Yuan;ZHOU Xiao [1]Rong;ZHANG [1]Meng;FANG [1]Qian;WANG Wen [1]Jun;CHEN [3]Chen;DENG Xiang [4]Hua;CHEN Jing [1]Hong 高影响力作者 机构地区：[1]Institute of Endemic Diseases,School of Public Health,Xi'an Jiaotong University Health Science Center,Key Laboratory of Trace Elements and Endemic Diseases,National Health and Family Planning Commission,Xi'an 710061,ShaanxL China;[2]Xi'an Jiaotong University Hospital,Xi'an 710049,ShaanxL China;[3]School of Biomedical Sciences,the University of Queensland,Brisbane 4072,Australia;[4]Laboratory for Soft Tissue Research,Hospital for Special Surgery,New York 10021,USA高影响力机构 出　　处：《Biomedical and Environmental Sciences》索引2017年第30卷第5期,共12页高影响力期刊 基　　金：supported by the National Natural Science Foundation of China(No.81573102 and No.81273006);the Scientific Research Foundation for the Returned Overseas Chinese Scholars,State Education Ministry(11-01) 摘　　要：Objective To investigate chondrocyte apoptosis and the expression of biochemical markers associated with apoptosis in Kashin-Beck disease(KBD) and in an established T-2 toxin-and selenium(Se) deficiency-induced rat model. Methods Cartilages were collected from the hand phalanges of five patients with KBD and five healthy children. Sprague-Dawley rats were administered a selenium-deficient diet for 4 weeks prior to T-2 toxin exposure. The apoptotic chondrocytes were observed by terminal deoxynucleotidyl transferase d UTP nick end labeling staining. Caspase-3, p53, Bcl-2, and Bax proteins in the cartilages were visualized by immunohistochemistry, their protein levels were determined by Western blotting, and m RNA levels were determined by real-time reverse transcription polymerase chain reaction. Results Increased chondrocyte apoptosis was observed in the cartilages of children with KBD. Increased apoptotic and caspase-3-stained cells were observed in the cartilages of rats fed with normal and Se-deficient diets plus T-2 toxin exposure compared to those in rats fed with normal and Se-deficient diets. Caspase-3, p53, and Bax proteins and m RNA levels were higher, whereas Bcl-2 levels were lower in rats fed with normal or Se-deficiency diets supplemented with T-2 toxin than the corresponding levels in rats fed with normal diet. Conclusion T-2 toxin under a selenium-deficient nutritional status induces chondrocyte death, which emphasizes the role of chondrocyte apoptosis in cartilage damage and progression of KBD. 关 键 词：KBD CHONDROCYTE APOPTOSIS T-2 toxin Selenium-deficiency
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