Carvedilol prevents pancreatic β-cell damage and the development of type 1 diabetes in mice by the inhibition of proinflammatory cytokines, NF-κB, COX-2, iNOS and oxidative stress

Cytokine ◽  
2021 ◽  
Vol 138 ◽  
pp. 155394
Author(s):  
Keyvan Amirshahrokhi ◽  
Ali Zohouri
Keyword(s):  
Oxidative Stress ◽  
Type 1 Diabetes ◽  
Proinflammatory Cytokines ◽  
Cell Damage ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Diabetes In Mice ◽  
Cox 2 ◽  
And Oxidative Stress

scholarly journals Inhibition of the Keap1/Nrf2 Signaling Pathway Significantly Promotes the Progression of Type 1 Diabetes Mellitus

2021 ◽  
Vol 2021 ◽  
pp. 1-19
Author(s):  
Yanmei Lou ◽  
Muyan Kong ◽  
Leyan Li ◽  
Yu Hu ◽  
Wenjun Zhai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Cell Damage ◽  
Pancreatic Β Cell ◽  
Β Cells ◽  
Β Cell ◽  
Pancreatic Β Cells ◽  
Min6 Cells ◽  
Nrf2 Signaling Pathway

Type 1 diabetes mellitus (T1DM) is an autoimmune disease characterized by insulin deficiency due to pancreatic β-cell damage and leads to hyperglycemia. The precise molecular mechanisms of the etiology of T1DM are not completely understood. Oxidative stress and the antioxidant status of pancreatic β-cells play a vital role in the pathogenesis and progression of T1DM. The Keap1/Nrf2 signaling pathway plays a critical role in cellular resistance to oxidative stress. This study is aimed at investigating the role of the Keap1/Nrf2 signaling pathway in the progression of T1DM. An alloxan- (ALX-) stimulated T1DM animal model in wild-type (WT) and Nrf2 knockout (Nrf2-/-) C57BL/6J mice and a mouse pancreatic β-cell line (MIN6) were established. Compared with the tolerant (ALX exposure, nondiabetic) WT mice, the sensitive (ALX exposure, diabetic) WT mice exhibited higher blood glucose levels and lower plasma insulin levels. The Keap1/Nrf2 signaling pathway was significantly inhibited in the sensitive WT mice, which was reflected by overexpression of Keap1 and low expression of Nrf2, accompanied by a marked decrease in the expression of the antioxidative enzymes. Compared with WT mice, the Nrf2-/- mice had an increased incidence of T1DM and exhibited more severe pancreatic β-cell damage. The results of in vitro experiments showed that ALX significantly inhibited the viability and proliferation and promoted the apoptosis of MIN6 cells. ALX also markedly increased intracellular ROS production and caused DNA damage in MIN6 cells. In addition, the Keap1/Nrf2 signaling pathway was significantly inhibited in the damaged MIN6 cells. Moreover, Nrf2 silencing by transfection with Nrf2 siRNA markedly exacerbated ALX-induced MIN6 cell injury. Conclusively, this study demonstrates that inhibition of the Keap1/Nrf2 signaling pathway could significantly promote the incidence of T1DM. This study indicates that activation of Keap1/Nrf2 signaling in pancreatic β-cells may be a useful pharmacological strategy for the clinical prevention and treatment of T1DM.

scholarly journals Cichorium intybus attenuates Streptozotocin-induced pancreatic β-cell damage by inhibiting NF-κB activation and oxidative stress

2020 ◽  
Vol 18 (2-3 double issue) ◽  
pp. 70-79
Author(s):  
Ramya Devi KT ◽  
Nageswaran Sivalingam
Keyword(s):  
Oxidative Stress ◽  
Cell Damage ◽  
Cichorium Intybus ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
And Oxidative Stress

scholarly journals Adipose‐Derived Stem Cells Ameliorate STZ‐Induced Pancreatic β Cell Damage in Type 1 Diabetes

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Yueying Li ◽  
Hanhan Liu ◽  
Yinping Li
Keyword(s):  
Stem Cells ◽  
Type 1 Diabetes ◽  
Cell Damage ◽  
Adipose Derived Stem Cells ◽  
Pancreatic Β Cell ◽  
Β Cell

The effect of oral folic acid upon plasma homocysteine, endothelial function and oxidative stress in patients with type 1 diabetes and microalbuminuria

2008 ◽  
Vol 62 (4) ◽  
pp. 569-574 ◽  
Author(s):  
F. Wotherspoon ◽  
D. W. Laight ◽  
C. Turner ◽  
D. R. Meeking ◽  
S. E. Allard ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 1 Diabetes ◽  
Folic Acid ◽  
Endothelial Function ◽  
Plasma Homocysteine ◽  
And Oxidative Stress

Type 1 diabetes and oxidative stress markers

2021 ◽  
Vol 242 ◽  
pp. 174
Author(s):  
Widad Sobhi ◽  
Rania Derguine ◽  
Saliha Boucheffa ◽  
Abdelhalim Khenchouche ◽  
Nada Boutrid ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 1 Diabetes ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
And Oxidative Stress

scholarly journals Nonlinear Analysis for a Type-1 Diabetes Model with Focus on T-Cells and Pancreatic β-Cells Behavior

2020 ◽  
Vol 25 (2) ◽  
pp. 23
Author(s):  
Diana Gamboa ◽  
Carlos E. Vázquez ◽  
Paul J. Campos
Keyword(s):  
T Cells ◽  
Type 1 Diabetes ◽  
Cell Population ◽  
Closed Loop ◽  
Pancreatic Β Cell ◽  
Activated Macrophages ◽  
Β Cells ◽  
Β Cell ◽  
Pancreatic Β Cells

Type-1 diabetes mellitus (T1DM) is an autoimmune disease that has an impact on mortality due to the destruction of insulin-producing pancreatic β -cells in the islets of Langerhans. Over the past few years, the interest in analyzing this type of disease, either in a biological or mathematical sense, has relied on the search for a treatment that guarantees full control of glucose levels. Mathematical models inspired by natural phenomena, are proposed under the prey–predator scheme. T1DM fits in this scheme due to the complicated relationship between pancreatic β -cell population growth and leukocyte population growth via the immune response. In this scenario, β -cells represent the prey, and leukocytes the predator. This paper studies the global dynamics of T1DM reported by Magombedze et al. in 2010. This model describes the interaction of resting macrophages, activated macrophages, antigen cells, autolytic T-cells, and β -cells. Therefore, the localization of compact invariant sets is applied to provide a bounded positive invariant domain in which one can ensure that once the dynamics of the T1DM enter into this domain, they will remain bounded with a maximum and minimum value. Furthermore, we analyzed this model in a closed-loop scenario based on nonlinear control theory, and proposed bases for possible control inputs, complementing the model with them. These entries are based on the existing relationship between cell–cell interaction and the role that they play in the unchaining of a diabetic condition. The closed-loop analysis aims to give a deeper understanding of the impact of autolytic T-cells and the nature of the β -cell population interaction with the innate immune system response. This analysis strengthens the proposal, providing a system free of this illness—that is, a condition wherein the pancreatic β -cell population holds and there are no antigen cells labeled by the activated macrophages.

Hydrophilic CeO2nanocubes protect pancreatic β-cell line INS-1 from H2O2-induced oxidative stress

Nanoscale ◽  
2016 ◽  
Vol 8 (15) ◽  
pp. 7923-7932 ◽  
Author(s):  
Guang-Ming Lyu ◽  
Yan-Jie Wang ◽  
Xue Huang ◽  
Huai-Yuan Zhang ◽  
Ling-Dong Sun ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Line ◽  
Hydrothermal Method ◽  
Cell Damage ◽  
Pancreatic Β Cell ◽  
Β Cell

Hydrophilic 5 nm and 25 nm CeO2nanocubes, synthesized from the convenient acetate assisted hydrothermal method, could be employed as greatly promising potential antioxidants for controlling H2O2-induced pancreatic β-cell damage.

Relationship between glucose control, glycemic variability, and oxidative stress in children with type 1 diabetes

2019 ◽  
Vol 66 (9) ◽  
pp. 540-549
Author(s):  
Natalia Colomo ◽  
Juan Pedro López-Siguero ◽  
Isabel Leiva ◽  
Noemí Fuentes ◽  
Elehazara Rubio-Martín ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 1 Diabetes ◽  
Glucose Control ◽  
Glycemic Variability ◽  
And Oxidative Stress

scholarly journals Dendritic Cell-Directed CTLA-4 Engagement during Pancreatic β Cell Antigen Presentation Delays Type 1 Diabetes

2010 ◽  
Vol 184 (12) ◽  
pp. 6695-6708 ◽  
Author(s):  
Subha Karumuthil-Melethil ◽  
Nicolas Perez ◽  
Ruobing Li ◽  
Bellur S. Prabhakar ◽  
Mark J. Holterman ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Dendritic Cell ◽  
Antigen Presentation ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Antigen
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