ABSTRACT
Objective To observe the effect of superoxide dismutase ( SOD ) , malondialdehyde ( MDA ) , glutathione (GSH), catalase (CAT) and endothelin (ET-1) and tumor necrosis factor alpha (TNF-α) on rat renal tissue under acute hypoxia .Methods 24 male Wistar rats, weight 180~220 g, were randomly divided into control group and acute hypobaric hypoxia group .Acute hypoxia group was divided into 2 groups hypoxia 1 and hypoxia 2, 8 rats for each group.After acute hypobaric hypoxia 10min and 24h, rats were sacrificed.The left removed kidneys were analyzed for biochemical indexes , and the right parts were observed by immunohistochemistry to evaluate the expression level of renal endothelin (ET-1) and tumor necrosis factor alpha (TNF-α).Results After acute hypobaric hypoxia , the activity of SOD of the rats kidney was greatly decreased (P 0.05).The immunohistochemical staining showed that , the expression level of ET-1 and TNF-αwas increased remarkably, but it was reduced after 24 h.Conclusion The obviously decreased activity of SOD , CAT, GSH and significantly increased expression of ET-1 and TNF-α, may be involved in the pathogenesis of renal hypoxic injury .
ABSTRACT
Recent studies have unequivocally established the link between FTO and obesity. FTO was biochemically shown to belong to the AlkB-like family DNA/RNA demethylase. However, FTO differs from other AlkB members in that it has unique substrate specificity and contains an extended C-terminus with unknown functions. Insight into the substrate selection mechanism and a functional clue to the C-terminus of FTO were gained from recent structural and biochemical studies. These data would be valuable to design FTO-specific inhibitors that can be potentially translated into therapeutic agents for treatment of obesity or obesity-related diseases.