Abstract
Background: Ginseng have been proposed to mediate antidiabetic effect. The active components of ginseng are thought to be ginsenoside and distributed in many parts of the ginseng plant. Rg3, one of the active ingredients of ginseng saponins, has been known about the effects on molecularmechanism related to diabetes including inhibition the palmitate-induced beta-cell apoptosis and enhancement the glucose uptake. Glucose variability could induce a higher degree of apoptosis and decreased the insulin secretory capacity in beta-cells. In the present study, we investigated whether Rg3 suppresses intermittent high glucose(IHG)induced beta-cell apoptosis and improved insulin secretion in INS-1 pancreatic beta-cells. Method: To perform Glucose Fluctuation and protection effect by ginsenoside Rg3, mediums were aspirated and new medium containing Glucose Fluctuation or/and Rg3 concentrations was added and incubated for 2days. Annexin V staining for apoptosis detection analyzed by FACsort. Cell viability was determined by CCK-8 assay. The optical density was measured at 450 nm by automatic plate reader. Quantification of secreted insulin protein by ELISA was measured using Rat/mouse Insulin ELISA kit. BrdU staining was added in and quantification of secreted insulin proteins were analyzed by FACSort. Result: After 48hrs, INS-1 cell treated with alternative high glucose concentration(33mM glucose) and low glucose concentration(5mM) increased beta-cells apoptosis by 5.37 fold. But culturing with Rg3 1mM, 5mM,10mM, the percentages of apoptotic cells were reduced by dose dependently. Cell viability was reduced 63% by IHG. This toxic effect was also attenuated by culturing with Rg3. Additionally, when we added BrdU to culture medium and labeling of proliferating cells, cell proliferation was tended to be increased. And the ratio of quantification of secreted insulin protein/total protein was also tended to be increased with Rg3 dose dependently. Conclusion: Ginsenoside Rg3 suppresses intermittent high glucose-induced apoptosis and increases cell viability. Also it has tendancy to increase cell proliferation and the ratio of insulin secreting protein/total protein in INS-1 pancreatic beta-cells.
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