Increased levels of IL-6, IL-1β, and TNF-α in Kashin–Beck disease and rats induced by T-2 toxin and selenium deficiency
文摘
The objective of this study is to investigate the possible role of inflammatory mediators such as IL-6, IL-1β, and TNF-α in Kashin–Beck disease (KBD) children and rats fed with T-2 toxin under a selenium-deficient nutrition status in order to determine possible mechanism underlying KBD. Sprague–Dawley rats were administered a selenium-deficient diet for 4?weeks prior to their exposure to T-2 toxin for 4?weeks. The morphology of joint cartilages of KBD children and rats was examined by light microscopy, and the expression of proteoglycans was determined by histochemical staining. The serum levels of IL-6, IL-1β, and TNF-α were determined by enzyme-linked immunosorbent assay. IL-6, IL-1β and TNF-α were localized by immunohistochemistry, and their mRNA levels were detected by real-time RT-PCR. The serum levels of IL-6 were significantly elevated in rats fed with selenium-deficient, T-2 toxin, and T-2 toxin plus selenium-deficient diets compared to those in the normal diet, while the serum levels of IL-1β and TNF-α were significantly increased only in the T-2 toxin plus selenium-deficient diet group. IL-6, IL-1β and TNF-α protein and mRNA levels in cartilage were significantly higher in rats with diets of T-2 toxin and T-2 toxin plus selenium deficiency than in rats fed normal or selenium-deficient diet. While staining for the cytokines in cartilages of KBD children was significantly higher than that in controls. T-2 toxin under a selenium-deficient nutritional status induces increased levels of IL-6, IL-1β, and TNF-α in serum and cartilages, which may account for the pathological mechanism underlying the cartilage damage in KBD.