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Updated: Mar 20, 2026
Homogeneous Time-resolved Förster Resonance Energy Transfer-based Assay for Detection of Insulin Secretion
Published on: May 10, 2018
Ginsenoside Rg3 prevents INS-1 cell death from intermittent high glucose stress
You Jeong Kim1, Su Min Park2, Hye Sook Jung3
1a Division of Endocrinology and Metabolism, Department of Internal Medicine, Maryknoll Medical Center , Busan , South Korea.
Background:
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.
Methods:
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.
Result:
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.
Conclusion:
Ginsenoside Rg3 protected INS-1 cell death from IHG with reducing apoptosis and increasing proliferation.
Insights
Ginsenoside Rg3 (Rg3) protects pancreatic beta cells from intermittent high glucose (IHG) by reducing cell death and enhancing proliferation. This study clarifies Rg3
Area of Science:
- Endocrinology
- Cell Biology
- Pharmacology
Background:
- Pancreatic beta cell dysfunction is central to diabetes.
- Intermittent high glucose (IHG) poses a significant threat to beta cell health.
- The protective mechanisms of ginsenoside Rg3 against IHG-induced damage remain unclear.
Purpose of the Study:
- To investigate the protective effects of ginsenoside Rg3 (Rg3) on pancreatic beta cells under IHG conditions.
- To elucidate the underlying mechanisms involving apoptosis, proliferation, and insulin secretion.
- To assess the role of mitogen-activated protein kinase (MAPK) pathways.
Main Methods:
- INS-1 cells were exposed to IHG with or without Rg3.
- Cell viability, apoptosis, and proliferation were assessed using MTT assay, Annexin V staining, and BrdU analysis.
- Insulin secretion was quantified using ELISA kits.
- MAPK pathway activation (ERK, p38) was analyzed via Western blotting.
Main Results:
- IHG decreased INS-1 cell viability and increased apoptosis, which were ameliorated by Rg3.
- Rg3 treatment significantly enhanced insulin secretion and promoted cell proliferation.
- Rg3 reversed the IHG-induced suppression of ERK and p38 MAPK pathways.
Conclusions:
- Ginsenoside Rg3 demonstrates significant protective effects against IHG-induced pancreatic beta cell damage.
- Rg3 mitigates apoptosis and boosts proliferation, thereby preserving beta cell function.
- The findings highlight Rg3 as a potential therapeutic agent for managing diabetes-related beta cell complications.
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