title: Ginsenoside Rg3 prevents INS-1 cell death from intermittent high glucose stress.
abstract: Ginsenoside Rg3 has been proposed to mediate anti-diabetic effects, but their direct effect on pancreatic β cell viability and mechanisms are not clearly understood. Recent studies suggest that intermittent high glucose (IHG) could be more harmful to pancreatic β cells than sustained high glucose. There are few reports about the effect of the ginsenosideRg3 to β cell apoptosis and proliferation against IHG.
  
  
  
  INS-1 cells were treated with alternative glucose concentration with or without ginsenoside Rg3. Cell apoptosis and viability were detected by Annexin V staining and MTT assay. The activation of mitogen-activated protein kinases (MAPKs) was analyzed by Western blotting using specific antibodies. Quantification of secreted insulin protein was measured using rat/mouse Insulin ELISA kits. Bromodeoxyuridine (BrdU) staining and florescence in situ hybridization (FISH) analysis was performed to compare cell proliferation.
  
  
  
  INS-1 cell viability was decreased under IHG and increased with Rg3 treatment.Rg3 significantly reduced the apoptotic INS-1 cells against IHG. The quantification of secreted insulin concentration was increased with Rg3. Rg3 increased INS-1 cell proliferation. ERK and p38 MAPK pathways reduced by IHG were activated by the ginsenoside Rg3.
  
  
  
  Ginsenoside Rg3 protected INS-1 cell death from IHG with reducing apoptosis and increasing proliferation.
authors.affiliation: a Division of Endocrinology and Metabolism, Department of Internal Medicine, Maryknoll Medical Center , Busan , South Korea.
authors.forename: You Jeong
authors.initials: YJ
authors.lastname: Kim
authors.affiliation: b Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, Inje University , Busan , South Korea.
authors.forename: Su Min
authors.initials: SM
authors.lastname: Park
authors.affiliation: c Paik Institute for Clinical Research, Molecular Therapy Lab, Inje University , Busan , South Korea.
authors.forename: Hye Sook
authors.initials: HS
authors.lastname: Jung
authors.affiliation: b Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, Inje University , Busan , South Korea.
authors.forename: Eun Ju
authors.initials: EJ
authors.lastname: Lee
authors.affiliation: b Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, Inje University , Busan , South Korea.
authors.forename: Tae Kyoon
authors.initials: TK
authors.lastname: Kim
authors.affiliation: b Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, Inje University , Busan , South Korea.
authors.forename: Tae-Nyun
authors.initials: TN
authors.lastname: Kim
authors.affiliation: b Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, Inje University , Busan , South Korea.
authors.forename: Min Jeong
authors.initials: MJ
authors.lastname: Kwon
authors.affiliation: b Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, Inje University , Busan , South Korea.
authors.forename: Soon Hee
authors.initials: SH
authors.lastname: Lee
authors.affiliation: b Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, Inje University , Busan , South Korea.
authors.forename: Byoung Doo
authors.initials: BD
authors.lastname: Rhee
authors.affiliation: b Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, Inje University , Busan , South Korea.|c Paik Institute for Clinical Research, Molecular Therapy Lab, Inje University , Busan , South Korea.
authors.forename: Mi-Kyung
authors.initials: MK
authors.lastname: Kim
authors.affiliation: b Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, Inje University , Busan , South Korea.|c Paik Institute for Clinical Research, Molecular Therapy Lab, Inje University , Busan , South Korea.
authors.forename: Jeong Hyun
authors.initials: JH
authors.lastname: Park
mesh_terms: D000818:Animals; D017304:Annexin A5 / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects; D015153:Blotting, Western; D016923:Cell Death / Q000187:drug effects*; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D036145:Ginsenosides / Q000008:administration & dosage / Q000494:pharmacology*; D005947:Glucose / Q000494:pharmacology*; D006801:Humans; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000187:drug effects*; D051381:Rats
chemical_list: D017304:Annexin A5; D036145:Ginsenosides; D007328:Insulin; C097367:ginsenoside Rg3; D005947:Glucose
keywords: anti-apoptosis; cell proliferation; cytoprotection; ginsenoside Rg3; insulin-secreting cells