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Rapid Determination of the Thermal Nociceptive Threshold in Diabetic Rats
Published on: May 17, 2012
Targeting tumor necrosis factor alpha (TNF-α) in diabetic rats could approve avenues for an efficient strategy for
Karolin K Abdul-Aziz1, Muobarak J Tuorkey
1Zoology Department, Division of Physiology, Damanhour University, Egypt. k.kamel2002@yahoo.com
Background:
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.
Aim:
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.
Methods:
Using western blot, IHC, Elisa, biochemical assays and scanning electron microscope.
Results:
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.
Conclusion:
Findings of this study reveal how TNF-α can be mechanistically coupled to greater diabetic complications potential.
Insights
Downregulating tumor necrosis factor-alpha (TNF-α) may help prevent diabetes complications. This study investigated long-term TNF-α inhibition, finding it mechanistically linked to increased diabetic complications.
Area of Science:
- Immunology
- Endocrinology
- Molecular Biology
Background:
- Tumor necrosis factor-alpha (TNF-α) downregulation is believed to prevent diabetes and its complications.
- Potential long-term adverse biological effects of TNF-α downregulation remain unclear.
Purpose of the Study:
- To investigate the impact of anti-TNF-α antibody treatment on biological activities after 4 weeks.
- To elucidate the mechanistic link between TNF-α and diabetic complications.
Main Methods:
- Western blot
- Immunohistochemistry (IHC)
- Enzyme-linked immunosorbent assay (ELISA)
- Biochemical assays
- Scanning electron microscopy
Main Results:
- TNF-α, FOXO-1, IL-6, and MPO collectively induce significant changes in diabetic rats.
- TNF-α activates transcription factor FOXO1, contributing to neutrophil-mediated oxidative stress.
- IL-6 exacerbates stress mediators via neutrophil activation; FOXO1 attempts to counteract this.
- Defects in IgA and IL-2 secretions may cause digestive atrophy.
- Akt-1 inhibits caspase 3, potentially preventing apoptosis.
Conclusions:
- TNF-α plays a mechanistic role in the development of diabetic complications.
- Understanding these pathways is crucial for managing diabetes and its sequelae.
