2012Basic & Clinical MedicineRequires access

Ghrelin inhibits palmitate-induced apoptosis in rat endothelial cells and its mechanism

Guoliang Liu

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Abstract

Objective To investigate the effect of ghrelin on palmitate-induced apoptosis in rat aortic endothelial cells and the potential involvement of PI3K/Akt pathway.Methods Rat aortic endothelial cells were cultured in DMEM containing 0.3 mmol/L palmitate,with ghrelin and PI3K/Akt inhibitor,LY294002.Apoptosis was detected using an annexin V-FITC/PI double staining assay.Spectrofluorometer assay caspase-3 activity.Western blot analysis was used to examine the expression of total Akt and P-Akt.Results The apoptosis rate of rat aortic endothelial cells in palmitate group is 30.30%±1.98%,which is significantly higher than that of the control group(5.01%±0.52%)(P0.01).The apoptosis rate of endothelial cells in the ghrelin and palmitate group is 10.03%±0.90%,which is significantly lower than that of the palmitate group(P0.01).Ghrelin induced Akt activation.PI3K inhibitor,LY294002 blocked Akt activation and alleviated the anti-apotosis effect of ghrelin in endothelial cells.Conclusions Ghrelin inhibits palmitate-induced apoptosis in rat aortic endothelial cells.The effect of ghrelin is potentially partly mediated by PI3K/Akt pathway.

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Objective To investigate the effect of ghrelin on palmitate-induced apoptosis in rat aortic endothelial cells and the potential involvement of PI3K/Akt pathway.Methods Rat aortic endothelial cells were cultured in DMEM containing 0.3 mmol/L palmitate,with ghrelin and PI3K/Akt inhibitor,LY294002.Apoptosis was detected using an annexin V-FITC/PI double staining assay.Spectrofluorometer assay caspase-3 activity.Western blot analysis was used to examine the expression of total Akt and P-Akt.Results The apoptosis rate of rat aortic endothelial cells in palmitate group is 30.30%±1.98%,which is significantly higher than that of the control group(5.01%±0.52%)(P0.01).The apoptosis rate of endothelial cells in the ghrelin and palmitate group is 10.03%±0.90%,which is significantly lower than that of the palmitate group(P0.01).Ghrelin induced Akt activation.PI3K inhibitor,LY294002 blocked Akt activation and alleviated the anti-apotosis effect of ghrelin in endothelial cells.Conclusions Ghrelin inhibits palmitate-induced apoptosis in rat aortic endothelial cells.The effect of ghrelin is potentially partly mediated by PI3K/Akt pathway.

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Available abstract

Objective To investigate the effect of ghrelin on palmitate-induced apoptosis in rat aortic endothelial cells and the potential involvement of PI3K/Akt pathway.Methods Rat aortic endothelial cells were cultured in DMEM containing 0.3 mmol/L palmitate,with ghrelin and PI3K/Akt inhibitor,LY294002.Apoptosis was detected using an annexin V-FITC/PI double staining assay.Spectrofluorometer assay caspase-3 activity.Western blot analysis was used to examine the expression of total Akt and P-Akt.Results The apoptosis rate of rat aortic endothelial cells in palmitate group is 30.30%±1.98%,which is significantly higher than that of the control group(5.01%±0.52%)(P0.01).The apoptosis rate of endothelial cells in the ghrelin and palmitate group is 10.03%±0.90%,which is significantly lower than that of the palmitate group(P0.01).Ghrelin induced Akt activation.PI3K inhibitor,LY294002 blocked Akt activation and alleviated the anti-apotosis effect of ghrelin in endothelial cells.Conclusions Ghrelin inhibits palmitate-induced apoptosis in rat aortic endothelial cells.The effect of ghrelin is potentially partly mediated by PI3K/Akt pathway.

Key concepts: Ghrelin, Protein kinase B, Apoptosis, PI3K/AKT/mTOR pathway, Internal medicine, Endocrinology, LY294002, Annexin

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