scholarly journals Oxidative Stress-Responsive Apoptosis Inducing Protein (ORAIP) Plays a Critical Role in High Glucose-Induced Apoptosis in Rat Cardiac Myocytes and Murine Pancreatic β-Cells

Cells ◽  
2017 ◽  
Vol 6 (4) ◽  
pp. 35 ◽  
Author(s):  
Takako Yao ◽  
Tsutomu Fujimura ◽  
Kimie Murayama ◽  
Ko Okumura ◽  
Yoshinori Seko
Keyword(s):  
Oxidative Stress ◽  
Cardiac Myocytes ◽  
High Glucose ◽  
Critical Role ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Induced Apoptosis ◽  
Rat Cardiac Myocytes

Delphinidin-induced autophagy protects pancreatic β cells against apoptosis resulting from high-glucose stress via AMPK signaling pathway

2019 ◽  
Vol 51 (12) ◽  
pp. 1242-1249 ◽  
Author(s):  
Dengni Lai ◽  
Mingyong Huang ◽  
Lingyan Zhao ◽  
Yan Tian ◽  
Yong Li ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
High Glucose ◽  
Cell Mass ◽  
Protective Role ◽  
Common Disease ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Ampk Signaling ◽  
Compound C ◽  
Induced Apoptosis

Abstract Hyperglycemia, a diagnostic characteristic of diabetes mellitus, is detrimental to pancreatic β cells. Delphinidin, a member of the anthocyanin family, inhibits glucose absorption, increases glucagon-like peptide-1 (GLP-1) secretion, and improves insulin secretion in diabetes. However, whether delphinidin plays a protective role in pancreatic β-cell mass and function is not clear. In this study, delphinidin was found to decrease the high-glucose-induced apoptosis of RIN-m5F pancreatic β cells. In addition, delphinidin induced autophagy in RIN-m5F cells under the normal and high-glucose conditions, while 3-methyladenine (3-MA) inhibition of autophagy significantly diminished the protective role of delphinidin against high-glucose-induced apoptosis of pancreatic β cells. Delphinidin also decreased the level of cleaved caspase 3 and increased the phosphorylation level of AMP-activated protein kinase α (AMPKα) Thr172. Compound C, an AMPK inhibitor, was found to decrease the ratio of LC3-II/LC3-I, and the apoptotic rate of high-glucose-injured cells was increased after treatment with delphinidin, indicating that delphinidin attenuated the negative effects of high-glucose stress to cells. In conclusion, our data demonstrate that delphinidin protects pancreatic β cells against high-glucose-induced injury by autophagy regulation via the AMPK signaling pathway. These findings might shed light on the underlying mechanisms of diabetes and help improve the prevention and therapy of this common disease.

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 Protective Effect of Siegesbeckia orientalis on Pancreatic β-Cells under High Glucose-Induced Glucotoxicity

2021 ◽  
Vol 11 (22) ◽  
pp. 10963
Author(s):  
Chi-Chang Chang ◽  
Jer-Yiing Houng ◽  
Shih-Wei Wang ◽  
Chin-Feng Hsuan ◽  
Yung-Chuan Lu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Insulin Secretion ◽  
Protective Effect ◽  
Normal Level ◽  
High Glucose ◽  
Glucose Concentration ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Siegesbeckia Orientalis

The glucotoxicity caused by long-term exposure of β-cells to high glucose (HG) conditions may lead to the generation of more reactive oxygen species (ROS), reduce the activity of antioxidant enzymes, cause cell damage and apoptosis, and induce insulin secretion dysfunction. Siegesbeckia orientalis linne is a traditional folk herbal medicine used to treat snake bites, rheumatoid arthritis, allergies, and immune deficiencies. In this study, we evaluated the protective effect of S. orientalis ethanol extract (SOE) on cell death and oxidative stress in RIN-m5f pancreatic β-cells stimulated by two HG concentrations (50–100 mM). In the cell viability assay, SOE could significantly increase the survival rate of pancreatic β-cells under HG-induced conditions. For the oxidative stress induced by HG condition, the treatment of SOE effectively reduced the ROS formation, increased the content of intracellular glutathione, and up-regulated the expression of antioxidant enzymes, catalase, superoxide dismutase, and glutathione peroxidase. As a result, the SOE treatment could decrease the glucotoxicity-mediated oxidative damage on RIN-m5F β-cells. Moreover, SOE had the function of regulating insulin secretion in pancreatic β-cells under different HG-mediated conditions. It could decrease the increasing intracellular insulin secretion under the low glucose concentration to normal level; while increase the decreasing intracellular insulin secretion under the relatively high glucose concentration to normal level. Taken together, this study suggests that SOE has a protective effect on pancreatic β-cells under the HG-stimulated glucotoxic environment.

Crucial roles of neuronatin in insulin secretion and high glucose-induced apoptosis in pancreatic β-cells

2008 ◽  
Vol 20 (5) ◽  
pp. 907-915 ◽  
Author(s):  
Myung Kuk Joe ◽  
Hyo Jung Lee ◽  
Young Ho Suh ◽  
Kyu Lee Han ◽  
Joo Hyun Lim ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
High Glucose ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Induced Apoptosis

Cyanidin-3-rutinoside protects INS-1 pancreatic β cells against high glucose-induced glucotoxicity by apoptosis

2018 ◽  
Vol 73 (7-8) ◽  
pp. 281-289 ◽  
Author(s):  
Kung-Ha Choi ◽  
Mi Hwa Park ◽  
Hyun Ah Lee ◽  
Ji-Sook Han
Keyword(s):  
Cell Death ◽  
High Glucose ◽  
Cell Damage ◽  
Therapeutic Effects ◽  
Dependent Manner ◽  
Pancreatic Β Cell ◽  
Β Cells ◽  
Β Cell ◽  
Pancreatic Β Cells ◽  
Induced Apoptosis

Abstract Exposure to high levels of glucose may cause glucotoxicity, leading to pancreatic β cell dysfunction, including cell apoptosis and impaired glucose-stimulated insulin secretion. The aim of this study was to explore the effect of cyanidin-3-rutinoside (C3R), a derivative of anthocyanin, on glucotoxicity-induced apoptosis in INS-1 pancreatic β cells. Glucose (30 mM) treatment induced INS-1 pancreatic β cell death, but glucotoxicity and apoptosis significantly decreased in cells treated with 50 μM C3R compared to that observed in 30 mM glucose-treated cells. Furthermore, hyperglycemia increased intracellular reactive oxygen species (ROS), lipid peroxidation, and nitric oxide (NO) levels, while C3R treatment reduced these in a dose-dependent manner. C3R also increased the activity of antioxidant enzymes, markedly reduced the expression of pro-apoptotic proteins (such as Bax, cytochrome c, caspase 9 and caspase 3), and increased the expression of the anti-apoptotic protein, Bcl-2, in hyperglycemia-exposed cells. Finally, cell death was examined using annexin V/propidium iodide staining, which revealed that C3R significantly reduced high glucose-induced apoptosis. In conclusion, C3R may have therapeutic effects against hyperglycemia-induced β cell damage in diabetes.

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