Down-regulation of ATF2 in the inhibition of T-2-toxin-induced chondrocyte apoptosis by selenium chondroitin sulfate nanoparticles
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.
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