Down-regulation of ATF2 in the inhibition of T-2-toxin-induced chondrocyte apoptosis by selenium chondroitin sulfate nanoparticles
- 2.8k Downloads
Selenium chondroitin sulfate nanoparticles (SeCS) with a size range of 30–200 nm were obtained in our previous study. Meanwhile, the up-regulated expression of ATF2 mRNA and protein levels could be observed in the cartilage from Kashin–Beck disease (KBD) patients. In this paper, we investigated the inhibition effect of SeCS on T-2-toxin-induced apoptosis of chondrocyte from KBD patients. Here, we found that when the chondrocytes were treated with T-2 toxin, the chondrocyte apoptosis performed in a concentration-dependent manner. The apoptosis of chondrocyte induced by T-2 toxin involved the increased levels of ATF2, JNK and p38 mRNAs and related protein expression. SeCS could partly block the T-2-toxin-induced chondrocyte apoptosis by decreasing the expression of ATF2, JNK and p38 mRNAs and p-JNK, p-38, ATF2 and p-ATF2 proteins. JNK and p38 pathways involved in the apoptosis of chondrocyte induced by T-2 toxin, and SeCS was efficient in the inhibition of chondrocyte apoptosis by T-2 toxin. These results suggested that SeCS had a potential for further prevention and treatment for KBD as well as other selenium deficiency disease.
KeywordsApoptosis T-2 toxin Kashin–Beck disease Selenium ATF2 Nanobiotechnology
This work was supported by the National Natural Scientific Foundation of China (30972556) and the Specialized Research Fund for the Doctoral Program of Higher Education of China (20090201110049), and the Academy of Finland (Grant no. 128117). We thank the orthopedic surgeons and nursing staff of the Department of Orthopaedics or Trauma in the Xi’an Red Cross Hospital, the second affiliated hospital of Xian Jiaotong University and Shaanxi Endemic Disease Hospital for support and cooperation in the collection of cartilage specimens.
Conflict of interest
The authors declare that they have no competing interests.
- An YH, Jia XF, Li XF, He J, Han SB, Zhang H (2010) Geological environment characteristics and etiology research on Kashin–Beck disease in China (Article in Chinese). Geol China 37:539–563Google Scholar
- Guan F, Li SY, Wang ZL, Yang HJ, Xue SH, Wang W, Song DQ, Zhou XR, Zhou W, Chen JH, Caterson B, Hughes C (2013) Histopathology of chondronecrosis development in knee articular cartilage in a rat model of Kashin–Beck disease using T-2 toxin and selenium deficiency conditions. Rheumatol Int 33:157–166CrossRefGoogle Scholar
- Guo X (2008) Progression and prospect of etiology and pathogenesis of Kashin–Beck disease in China (Article in Chinese). Chin J Endemiol 27:6–8Google Scholar
- Han J, Guo X, Wu CY, Li CY, He SL, Duan C, Ning YJ (2013a) Nano-Se-chondroitin sulfate inhibits T-2 toxin-induced apoptosis of cultured chondrocytes from patients with Kashin–Beck disease (Article in Chinese). J Southern Medical Univ 33:225–229Google Scholar
- Mo DX (1979) Electron microscope of Kashin–Beck patients with articular cartilage and epiphyseal cartilage chondrocytes (Article in Chinese). J Xi’an Jiaotong Univ (Med Sci) 3:34–39Google Scholar
- Yang JB, Sun DJ, Wang ZW (1995) Determination of T-2 toxin in the staple food from the sick families in Kashin–Beck Disease (KBD) area (Article in Chinese). Chin J Endemiol 14:200–204Google Scholar