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

作　　者：YANG Hao Jie ZHANG Ying WANG Zhi Lun XUE Sen Hai LI Si Yuan ZHOU Xiao Rong ZHANG Meng FANG Qian WANG Wen Jun CHEN Chen DENG Xiang Hua CHEN Jing Hong 

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

出　　处：《Biomedical and Environmental Sciences》2017年第5期351-362,共12页生物医学与环境科学（英文版）

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.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 

分 类 号：R684[医药卫生—骨科学]