Protopanaxadiol ameliorates palmitate-induced lipotoxicity and pancreatic β-cell dysfunction in INS-1 cells

Background: Free fatty acid-induced lipotoxicity is considered to play an important role in pancreatic β-cell dysfunction. The effect of ginsenosides on palmitic acid-induced pancreatic beta-cells cell death and failure of glucose-stimulated secretion of insulin (GSIS) was evaluated in this study. M...

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Main Authors: Dahae Lee, Sungyoul Choi, Ki Sung Kang
Format: Article
Language:English
Published: Elsevier 2023-07-01
Series:Journal of Ginseng Research
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S1226845323000210
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author Dahae Lee
Sungyoul Choi
Ki Sung Kang
author_facet Dahae Lee
Sungyoul Choi
Ki Sung Kang
author_sort Dahae Lee
collection DOAJ
description Background: Free fatty acid-induced lipotoxicity is considered to play an important role in pancreatic β-cell dysfunction. The effect of ginsenosides on palmitic acid-induced pancreatic beta-cells cell death and failure of glucose-stimulated secretion of insulin (GSIS) was evaluated in this study. Methods: Enzyme-linked immunosorbent assay kit for a rat insulin was used to quantify glucose-stimulated insulin secretion. Protein expression was examined by western blotting analysis. Nuclear condensation was measured by staining with Hoechst 33342 stain. Apoptotic cell death was assessed by staining with Annexin V. Oil Red O staining was used to measure lipid accumulation. Results: We screened ginsenosides to prevent palmitic acid-induced cell death and impairment of GSIS in INS-1 pancreatic β-cells and identified protopanaxadiol (PPD) as a potential therapeutic agent. The protection effect of PPD was likely due to a reduction in apoptosis and lipid accumulation. PPD attenuated the palmitic acid-induced increase in the levels of B-cell lymphoma-2-associated X/B-cell lymphoma 2, poly (ADP-ribose) polymerase and cleaved caspase-3. Moreover, PPD prevented palmitic acid-induced impairment of insulin secretion, which was accompanied by an increase in the activation of phosphatidylinositol 3-kinase, peroxisome proliferator-activated receptor γ, insulin receptor substrate-2, serine-threonine kinase, and pancreatic and duodenal homeobox-1. Conclusion: Our results suggest that the protective effect of PPD on lipotoxicity and lipid accumulation induced by palmitic acid in pancreatic β-cells.
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spelling doaj.art-14021da0726d4ec8baa9b9ee18ee0ba72023-06-16T05:08:32ZengElsevierJournal of Ginseng Research1226-84532023-07-01474572582Protopanaxadiol ameliorates palmitate-induced lipotoxicity and pancreatic β-cell dysfunction in INS-1 cellsDahae Lee0Sungyoul Choi1Ki Sung Kang2College of Korean Medicine, Gachon University, Seongnam, Republic of KoreaCorresponding authors. College of Korean Medicine, Gachon University, Seongnam, 13120, Republic of Korea.; College of Korean Medicine, Gachon University, Seongnam, Republic of KoreaCorresponding authors. College of Korean Medicine, Gachon University, Seongnam, 13120, Republic of Korea.; College of Korean Medicine, Gachon University, Seongnam, Republic of KoreaBackground: Free fatty acid-induced lipotoxicity is considered to play an important role in pancreatic β-cell dysfunction. The effect of ginsenosides on palmitic acid-induced pancreatic beta-cells cell death and failure of glucose-stimulated secretion of insulin (GSIS) was evaluated in this study. Methods: Enzyme-linked immunosorbent assay kit for a rat insulin was used to quantify glucose-stimulated insulin secretion. Protein expression was examined by western blotting analysis. Nuclear condensation was measured by staining with Hoechst 33342 stain. Apoptotic cell death was assessed by staining with Annexin V. Oil Red O staining was used to measure lipid accumulation. Results: We screened ginsenosides to prevent palmitic acid-induced cell death and impairment of GSIS in INS-1 pancreatic β-cells and identified protopanaxadiol (PPD) as a potential therapeutic agent. The protection effect of PPD was likely due to a reduction in apoptosis and lipid accumulation. PPD attenuated the palmitic acid-induced increase in the levels of B-cell lymphoma-2-associated X/B-cell lymphoma 2, poly (ADP-ribose) polymerase and cleaved caspase-3. Moreover, PPD prevented palmitic acid-induced impairment of insulin secretion, which was accompanied by an increase in the activation of phosphatidylinositol 3-kinase, peroxisome proliferator-activated receptor γ, insulin receptor substrate-2, serine-threonine kinase, and pancreatic and duodenal homeobox-1. Conclusion: Our results suggest that the protective effect of PPD on lipotoxicity and lipid accumulation induced by palmitic acid in pancreatic β-cells.http://www.sciencedirect.com/science/article/pii/S1226845323000210ginsenosidesprotopanaxadiolpalmitic acidlipotoxicityapoptosis
spellingShingle Dahae Lee
Sungyoul Choi
Ki Sung Kang
Protopanaxadiol ameliorates palmitate-induced lipotoxicity and pancreatic β-cell dysfunction in INS-1 cells
Journal of Ginseng Research
ginsenosides
protopanaxadiol
palmitic acid
lipotoxicity
apoptosis
title Protopanaxadiol ameliorates palmitate-induced lipotoxicity and pancreatic β-cell dysfunction in INS-1 cells
title_full Protopanaxadiol ameliorates palmitate-induced lipotoxicity and pancreatic β-cell dysfunction in INS-1 cells
title_fullStr Protopanaxadiol ameliorates palmitate-induced lipotoxicity and pancreatic β-cell dysfunction in INS-1 cells
title_full_unstemmed Protopanaxadiol ameliorates palmitate-induced lipotoxicity and pancreatic β-cell dysfunction in INS-1 cells
title_short Protopanaxadiol ameliorates palmitate-induced lipotoxicity and pancreatic β-cell dysfunction in INS-1 cells
title_sort protopanaxadiol ameliorates palmitate induced lipotoxicity and pancreatic β cell dysfunction in ins 1 cells
topic ginsenosides
protopanaxadiol
palmitic acid
lipotoxicity
apoptosis
url http://www.sciencedirect.com/science/article/pii/S1226845323000210
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AT sungyoulchoi protopanaxadiolamelioratespalmitateinducedlipotoxicityandpancreaticbcelldysfunctioninins1cells
AT kisungkang protopanaxadiolamelioratespalmitateinducedlipotoxicityandpancreaticbcelldysfunctioninins1cells