scholarly journals Platycodin D protects pancreatic β-cells from STZ-induced oxidative stress and apoptosis

2021 ◽  
Author(s):  
Yuan QIAO ◽  
Lingling ZHANG ◽  
Chunyang HOU ◽  
Fangzhi LI
Keyword(s):  
Oxidative Stress ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Platycodin D

scholarly journals Synergistic Effects of Milk-Derived Exosomes and Galactose on α-Synuclein Pathology in Parkinson’s Disease and Type 2 Diabetes Mellitus

2021 ◽  
Vol 22 (3) ◽  
pp. 1059
Author(s):  
Bodo C. Melnik
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Dopaminergic Neurons ◽  
Vagal Nerve ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
The Brain

Epidemiological studies associate milk consumption with an increased risk of Parkinson’s disease (PD) and type 2 diabetes mellitus (T2D). PD is an α-synucleinopathy associated with mitochondrial dysfunction, oxidative stress, deficient lysosomal clearance of α-synuclein (α-syn) and aggregation of misfolded α-syn. In T2D, α-syn promotes co-aggregation with islet amyloid polypeptide in pancreatic β-cells. Prion-like vagal nerve-mediated propagation of exosomal α-syn from the gut to the brain and pancreatic islets apparently link both pathologies. Exosomes are critical transmitters of α-syn from cell to cell especially under conditions of compromised autophagy. This review provides translational evidence that milk exosomes (MEX) disturb α-syn homeostasis. MEX are taken up by intestinal epithelial cells and accumulate in the brain after oral administration to mice. The potential uptake of MEX miRNA-148a and miRNA-21 by enteroendocrine cells in the gut, dopaminergic neurons in substantia nigra and pancreatic β-cells may enhance miRNA-148a/DNMT1-dependent overexpression of α-syn and impair miRNA-148a/PPARGC1A- and miRNA-21/LAMP2A-dependent autophagy driving both diseases. MiRNA-148a- and galactose-induced mitochondrial oxidative stress activate c-Abl-mediated aggregation of α-syn which is exported by exosome release. Via the vagal nerve and/or systemic exosomes, toxic α-syn may spread to dopaminergic neurons and pancreatic β-cells linking the pathogenesis of PD and T2D.

scholarly journals Cytoprotective Effects of N-Acetylcysteine on Streptozotocin- Induced Oxidative Stress and Apoptosis in RIN-5F Pancreatic β-Cells

2018 ◽  
Vol 51 (1) ◽  
pp. 201-216 ◽  
Author(s):  
Arwa M.T. Al-Nahdi ◽  
Annie John ◽  
Haider  Raza
Keyword(s):  
Oxidative Stress ◽  
Insulin Secretion ◽  
Molecular Mechanisms ◽  
Protective Action ◽  
Mitochondrial Enzymes ◽  
Partial Recovery ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Mitochondrial Energy Metabolism ◽  
Mitochondrial Functions

Background/Aims: Numerous studies have reported overproduction of reactive oxygen species (ROS) and alterations in mitochondrial energy metabolism in the development of diabetes and its complications. The potential protective effects of N-acetylcysteine (NAC) in diabetes have been reported in many therapeutic studies. NAC has been shown to reduce oxidative stress and enhance redox potential in tissues protecting them against oxidative stress associated complications in diabetes. In the current study, we aimed to investigate the molecular mechanisms of the protective action of NAC on STZ-induced toxicity in insulin secreting Rin-5F pancreatic β-cells. Methods: Rin-5F cells were grown to 80% confluence and then treated with 10mM STZ for 24h in the presence or absence of 10mM NAC. After sub-cellular fractionation, oxidative stress, GSH-dependent metabolism and mitochondrial respiratory functions were studied using spectrophotometric, flow cytometric and Western blotting techniques. Results: Our results showed that STZ-induced oxidative stress and apoptosis caused inhibition in insulin secretion while NAC treatment restored the redox homeostasis, enhanced insulin secretion in control cells and prevented apoptosis in STZ-treated cells. Moreover, NAC attenuated the inhibition of mitochondrial functions induced by STZ through partial recovery of the mitochondrial enzymes and restoration of membrane potential. STZ-induced DNA damage and expression of apoptotic proteins were significantly inhibited in NAC-treated cells. Conclusion: Our results suggest that the cytoprotective action of NAC is mediated via suppression of oxidative stress and apoptosis and restoration of GSH homeostasis and mitochondrial bioenergetics. This study may, thus, help in better understanding the cellular defense mechanisms of pancreatic β-cells against STZ-induced cytotoxicity.

Bach1 deficiency protects pancreatic β-cells from oxidative stress injury

2013 ◽  
Vol 305 (5) ◽  
pp. E641-E648 ◽  
Author(s):  
Keiichi Kondo ◽  
Yasushi Ishigaki ◽  
Junhong Gao ◽  
Tetsuya Yamada ◽  
Junta Imai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Pancreatic Islets ◽  
Antioxidative Enzymes ◽  
Heme Oxygenase 1 ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Stress Injury ◽  
Induced Apoptosis ◽  
Deficient Mice

BTB and CNC homology 1 (Bach1) is a transcriptional repressor of antioxidative enzymes, such as heme oxygenase-1 (HO-1). Oxidative stress is reportedly involved in insulin secretion impairment and obesity-associated insulin resistance. However, the role of Bach1 in the development of diabetes is unclear. HO-1 expression in the liver, white adipose tissue, and pancreatic islets was markedly upregulated in Bach1-deficient mice. Unexpectedly, glucose and insulin tolerance tests showed no differences in obese wild-type (WT) and obese Bach1-deficient mice after high-fat diet loading for 6 wk, suggesting minimal roles of Bach1 in the development of insulin resistance. In contrast, Bach1 deficiency significantly suppressed alloxan-induced pancreatic insulin content reduction and the resultant glucose elevation. Furthermore, TUNEL-positive cells in pancreatic islets of Bach1-deficient mice were markedly decreased, by 60%, compared with those in WT mice. HO-1 expression in islets was significantly upregulated in alloxan-injected Bach1-deficient mice, whereas expression of other antioxidative enzymes, e.g., catalase, superoxide dismutase, and glutathione peroxidase, was not changed by either alloxan administration or Bach1 deficiency. Our results suggest that Bach1 deficiency protects pancreatic β-cells from oxidative stress-induced apoptosis and that the enhancement of HO-1 expression plays an important role in this protection.

scholarly journals Reducing sugars trigger oxidative modification and apoptosis in pancreatic β-cells by provoking oxidative stress through the glycation reaction

1996 ◽  
Vol 320 (3) ◽  
pp. 855-863 ◽  
Author(s):  
Hideaki KANETO ◽  
Junichi FUJII ◽  
Theingi MYINT ◽  
Nobuko MIYAZAWA ◽  
Kazi N. ISLAM ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Cleavage ◽  
Reducing Sugars ◽  
Islet Cells ◽  
Chromatin Condensation ◽  
Oxidative Modification ◽  
Lipid Peroxidation Product ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Peroxidation Product

Several reducing sugars brought about apoptosis in isolated rat pancreatic islet cells and in the pancreatic β-cell-derived cell line HIT. This apoptosis was characterized biochemically by internucleosomal DNA cleavage and morphologically by nuclear shrinkage, chromatin condensation and apoptotic body formation. N-Acetyl-l-cysteine, an antioxidant, and aminoguanidine, an inhibitor of the glycation reaction, inhibited this apoptosis. We also showed directly that proteins in β-cells were actually glycated by using an antibody which can specifically recognize proteins glycated by fructose, but not by glucose. Furthermore, fluorescence-activated cell sorting analysis using dichlorofluorescein diacetate showed that reducing sugars increased intracellular peroxide levels prior to the induction of apoptosis. Levels of carbonyl, an index of oxidative modification, and of malondialdehyde, a lipid peroxidation product, were also increased. Taken together, these results suggest that reducing sugars trigger oxidative modification and apoptosis in pancreatic β-cells by provoking oxidative stress mainly through the glycation reaction, which may explain the deterioration of β-cells under conditions of diabetes.

scholarly journals Mitochondria-targeted Antioxidants Protect Pancreatic β-cells against Oxidative Stress and Improve Insulin Secretion in Glucotoxicity and Glucolipotoxicity

2011 ◽  
Vol 28 (5) ◽  
pp. 873-886 ◽  
Author(s):  
Sangbin Lim ◽  
Md Abdur Rashid ◽  
Miran Jang ◽  
Yeonghwan Kim ◽  
Hyeran Won ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Secretion ◽  
Β Cells ◽  
Pancreatic Β Cells

scholarly journals Suppression of KATP channel activity protects murine pancreatic β cells against oxidative stress

2009 ◽  
Author(s):  
Belinda Gier ◽  
Peter Krippeit-Drews ◽  
Tatiana Sheiko ◽  
Lydia Aguilar-Bryan ◽  
Joseph Bryan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Katp Channel ◽  
Channel Activity ◽  
Β Cells ◽  
Pancreatic Β Cells

The mitochondrial antioxidant MitoQ alleviates oxidative stress, endoplasmic reticulum stress and mitochondrial function in pancreatic β cells under hyperglycaemic conditions

2018 ◽  
Vol 120 ◽  
pp. S79-S80
Author(s):  
Irene Escribano-López ◽  
Noelia Dàz-Morales ◽  
Aranzazú M de Marañón ◽  
Francesca Iannantuoni ◽  
Sandra López-Domenech ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Mitochondrial Function ◽  
Β Cells ◽  
Pancreatic Β Cells
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