作者: Atilla Cayir , RA Ugan , Abdulmecit Albayrak , D Kose , Erol Akpinar
DOI: 10.1007/S40618-015-0282-Y
关键词:
摘要: The aim of this study is to show the effect a new mechanism on endothelin (ET) receptors in physiopathology diabetes-related pulmonary injury. We tested hypothesis that dual ET-1 receptor antagonism via bosentan can reverse diabetes-induced lung rats (24 male) were separated into four groups: group 1 (HEALTHY): Control group; 2 (DM): Streptozotocin 60 mg/kg (i.p.); 3 (DM + BOS-1): Diabetes + bosentan 50 mg/kg per-os; 4 (DM + BOS-2): 100 mg/kg per-os. treatment was initiated immediately after onset STZ-induced diabetes and continued for 6 weeks. In group, SOD activity significantly increased, although GSH MDA levels TNF-α TGF-β gene expression decreased. Bosentan showed down-regulatory ET-1, ET-A, ET-B mRNA expression. conclusion, increased associated with may be one cause endothelial dysfunction, cytokine increase, oxidant/antioxidant imbalance pathogenesis complications develop during diabetes. With its multiple effects, therapy an effective option against association