Sargassum sagamianum extract protects INS-1 pancreatic β cells against high glucose-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.

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

Cellular Signalling ◽

10.1016/j.cellsig.2008.01.005 ◽

2008 ◽

Vol 20 (5) ◽

pp. 907-915 ◽

Cited By ~ 40

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

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

Zeitschrift für Naturforschung C ◽

10.1515/znc-2017-0172 ◽

2018 ◽

Vol 73 (7-8) ◽

pp. 281-289 ◽

Cited By ~ 1

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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The protective effects and genetic pathways of thorn grape seeds oil against high glucose-induced apoptosis in pancreatic β-cells

BMC Complementary and Alternative Medicine ◽

10.1186/1472-6882-14-10 ◽

2014 ◽

Vol 14 (1) ◽

Cited By ~ 10

Author(s):

Xihu Lai ◽

Xincong Kang ◽

Luman Zeng ◽

Jian Li ◽

Yan Yang ◽

...

Keyword(s):

High Glucose ◽

Protective Effects ◽

Grape Seeds ◽

Β Cells ◽

Pancreatic Β Cells ◽

Genetic Pathways ◽

Induced Apoptosis

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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 ◽

10.3390/cells6040035 ◽

2017 ◽

Vol 6 (4) ◽

pp. 35 ◽

Cited By ~ 9

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

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HM-Chromanone Isolated from Portulaca oleracea L. Protects INS-1 Pancreatic β Cells against Glucotoxicity-Induced Apoptosis

Nutrients ◽

10.3390/nu11020404 ◽

2019 ◽

Vol 11 (2) ◽

pp. 404 ◽

Cited By ~ 1

Author(s):

Jae Eun Park ◽

Youngwan Seo ◽

Ji Sook Han

Keyword(s):

Protein Expression ◽

Cell Viability ◽

High Glucose ◽

Annexin V ◽

Thiobarbituric Acid ◽

Portulaca Oleracea ◽

Β Cells ◽

Pancreatic Β Cells ◽

Induced Apoptosis ◽

High Level

In this study, we investigated whether (E)-5-hydroxy-7-methoxy-3-(2′-hydroxybenzyl)-4-chromanone, a homoisoflavonoid compound isolated from Portulaca oleracea L., protects INS-1 pancreatic β cells against glucotoxicity-induced apoptosis. Treatment with high glucose (30 mM) induced apoptosis in INS-1 pancreatic β cells; however, the level of cell viability was significantly increased by treatment with (E)-5-hydroxy-7-methoxy-3-(2′-hydroxybenzyl)-4-chromanone. Treatment with 10–20 µM of (E)-5-hydroxy-7-methoxy-3-(2′-hydroxybenzyl)-4-chromanone dose-dependently increased cell viability and significantly decreased the intracellular level of reactive oxygen species (ROS), thiobarbituric acid reactive substances (TBARS), and nitric oxide levels in INS-1 pancreatic β cells pretreated with high glucose. These effects were associated with increased anti-apoptotic Bcl-2 protein expression, while reducing pro-apoptotic Bax, cytochrome C, and caspase 9 protein expression. Treatment with (E)-5-hydroxy-7-methoxy-3-(2′-hydroxybenzyl)-4-chromanone reduced the apoptosis previously induced by high-level glucose-treatment, according to annexin V/propidium iodide staining. These results demonstrate that (E)-5-hydroxy-7-methoxy-3-(2′-hydroxybenzyl)-4-chromanone may be useful as a potential therapeutic agent to protect INS-1 pancreatic β cells against high glucose-induced apoptosis.

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