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Increased Chondrocyte Apoptosis in Kashin-Beck Disease and Rats Induced by T-2 Toxin and Selenium Deficiency.
Biomed Environ Sci. 2017 May; 30(5):351-362.BE

Abstract

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 dUTP 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 mRNA 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 mRNA 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.

Authors+Show Affiliations

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, Shaanxi, China; Xi'an Jiaotong University Hospital, Xi'an 710049, Shaanxi, China.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, Shaanxi, China.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, Shaanxi, China.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, Shaanxi, China.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, Shaanxi, China.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, Shaanxi, China.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, Shaanxi, China.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, Shaanxi, China.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, Shaanxi, China.School of Biomedical Sciences, the University of Queensland, Brisbane 4072, Australia.Laboratory for Soft Tissue Research, Hospital for Special Surgery, New York 10021, USA.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, Shaanxi, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28549491

Citation

Yang, Hao Jie, et al. "Increased Chondrocyte Apoptosis in Kashin-Beck Disease and Rats Induced By T-2 Toxin and Selenium Deficiency." Biomedical and Environmental Sciences : BES, vol. 30, no. 5, 2017, pp. 351-362.
Yang HJ, Zhang Y, Wang ZL, et al. Increased Chondrocyte Apoptosis in Kashin-Beck Disease and Rats Induced by T-2 Toxin and Selenium Deficiency. Biomed Environ Sci. 2017;30(5):351-362.
Yang, H. J., Zhang, Y., Wang, Z. L., Xue, S. H., Li, S. Y., Zhou, X. R., Zhang, M., Fang, Q., Wang, W. J., Chen, C., Deng, X. H., & Chen, J. H. (2017). Increased Chondrocyte Apoptosis in Kashin-Beck Disease and Rats Induced by T-2 Toxin and Selenium Deficiency. Biomedical and Environmental Sciences : BES, 30(5), 351-362. https://doi.org/10.3967/bes2017.046
Yang HJ, et al. Increased Chondrocyte Apoptosis in Kashin-Beck Disease and Rats Induced By T-2 Toxin and Selenium Deficiency. Biomed Environ Sci. 2017;30(5):351-362. PubMed PMID: 28549491.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Increased Chondrocyte Apoptosis in Kashin-Beck Disease and Rats Induced by T-2 Toxin and Selenium Deficiency. AU - Yang,Hao Jie, AU - Zhang,Ying, AU - Wang,Zhi Lun, AU - Xue,Sen Hai, AU - Li,Si Yuan, AU - Zhou,Xiao Rong, AU - Zhang,Meng, AU - Fang,Qian, AU - Wang,Wen Jun, AU - Chen,Chen, AU - Deng,Xiang Hua, AU - Chen,Jing Hong, PY - 2016/09/30/received PY - 2017/03/02/accepted PY - 2017/5/28/entrez PY - 2017/5/28/pubmed PY - 2017/8/25/medline KW - Apoptosis KW - Chondrocyte KW - KBD KW - Selenium-deficiency KW - T-2 toxin SP - 351 EP - 362 JF - Biomedical and environmental sciences : BES JO - Biomed. Environ. Sci. VL - 30 IS - 5 N2 - 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 dUTP 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 mRNA 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 mRNA 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. SN - 0895-3988 UR - https://www.unboundmedicine.com/medline/citation/28549491/Increased_Chondrocyte_Apoptosis_in_Kashin_Beck_Disease_and_Rats_Induced_by_T_2_Toxin_and_Selenium_Deficiency_ L2 - https://doi.org/10.3967/bes2017.046 DB - PRIME DP - Unbound Medicine ER -