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• W2029165738 abstract "Aims To explore the effect and mechanism of exendin-4 on dexamethasone-induced apoptosis in pancreatic β-cells. Methods Murine MIN6 pancreatic β-cells were treated with dexamethasone (100 nmol/l) over 48 h following pretreatment with exendin-4 (100 nmol/l). Cell viability was determined using an MTT assay. The percentage of apoptotic cells was determined through fluorescence microscopy analysis after Hochest/PI staining and a flow cytometric assay after Annexin V-FITC/PI staining. Caspase 3 activity was measured using the caspase 3 activity assay kit. Expression of cyt-c, bcl-2, bax, AKT, and phosphorylated AKT was detected by western blot. Results Exendin-4 reduced the percentage of cells undergoing apoptosis when β-cells were exposed to dexamethasone. Exendin-4 down-regulated caspase 3 activity, reduced cytochrome c levels in cytoplasm, and increased Bcl-2 protein levels and the Bcl-2 to Bax ratio in dexamethasone-treated β-cells. These exendin-4 effects were blocked in the presence of an inhibitor of the phosphoinositide-3 kinase (PI-3K) pathway or of the protein kinase A (PKA) pathway. Exendin-4 reversed dexamethasone-mediated inhibition of Akt phosphorylation, which was abrogated by the PI-3K and PKA inhibitors. Conclusion PI-3K and PKA signaling are involved in the exendin-4-mediated modulation of β-cell apoptosis." @default.
• W2029165738 created "2016-06-24" @default.
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• W2029165738 date "2010-12-01" @default.
• W2029165738 modified "2023-10-16" @default.
• W2029165738 title "Exendin-4 protects murine pancreatic β-cells from dexamethasone-induced apoptosis through PKA and PI-3K signaling" @default.
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• W2029165738 doi "https://doi.org/10.1016/j.diabres.2010.09.004" @default.
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