Abstract
Several studies held belief that downregulation of TNF-α may be effective for preventing diabetes and it's complications. However, it is not known whether TNF-α downregulation in long-term can generate any biological adverse. The aim of the present study was to clarify what the impact is for such treatment with specific antibody for TNF-α on the other biological activities after 4weeks. Using western blot, IHC, Elisa, biochemical assays and scanning electron microscope. Results show that TNF-α, FOXO-1, IL-6 and MPO, when expressed in diabetic rats, collectively induce dramatic changes in diabetic rats. Since, TNF-α is involved in activation of transcription factor FOXO1 along with oxidative stress mediated by neutrophils. On one hand, IL-6 mediates neutrophils activation leading to an augmentation in stress mediators. And FOXO1 is activated in order to eliminate these oxidative mediators, on the other hand. Data show also that the prominent defect in mucosal IgA and IL-2 secretions may be the leading reasons for digestive atrophy. Finally, Akt-1 inhibits the cleavage of caspase 3, so, it could prevent the incidence of apoptosis. Findings of this study reveal how TNF-α can be mechanistically coupled to greater diabetic complications potential.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call