Increased Chondrocyte Apoptosis in Kashin-Beck Disease and Rats Induced by T-2 Toxin and Selenium Deficiency.
- Author:
Hao Jie YANG
1
,
2
;
Ying ZHANG
3
;
Zhi Lun WANG
3
;
Sen Hai XUE
3
;
Si Yuan LI
3
;
Xiao Rong ZHOU
3
;
Meng ZHANG
3
;
Qian FANG
3
;
Wen Jun WANG
3
;
Chen CHEN
4
;
Xiang Hua DENG
5
;
Jing Hong CHEN
3
Author Information
- Publication Type:Journal Article
- Keywords: Apoptosis; Chondrocyte; KBD; Selenium-deficiency; T-2 toxin
- MeSH: Adolescent; Animals; Apoptosis; drug effects; Biomarkers; Cartilage, Articular; physiopathology; Child; Chondrocytes; physiology; Female; Humans; Kashin-Beck Disease; etiology; physiopathology; Male; Matrilin Proteins; genetics; metabolism; Models, Animal; Random Allocation; Rats; Rats, Sprague-Dawley; Selenium; deficiency; T-2 Toxin; pharmacology
- From: Biomedical and Environmental Sciences 2017;30(5):351-362
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo 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.
METHODSCartilages 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.
RESULTSIncreased 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.
CONCLUSIONT-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.