Ghrelin inhibits AGEs-induced apoptosis in human endothelial cells involving ERK1/2 and PI3K/Akt pathways

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Xiang, Y., Q. Li, et al. (2011). "Ghrelin inhibits AGEs-induced apoptosis in human endothelial cells involving ERK1/2 and PI3K/Akt pathways." Cell Biochem Funct 29(two): 149-155.


Endothelial dysfunction caused by cell apoptosis is thought to be a key cause of diabetic vascular issues. Sophisticated glycation end merchandise (AGEs) play an important part in the pathogenesis of diabetic vascular difficulties by inducing apoptosis of endothelial cells. The goal of this study was to explore the effect of ghrelin on AGEs-induced apoptosis in cultured human umbilical vein endothelial cells (HUVECs) plus the possible mechanisms associated with this process. Exposure to AGEs (200 mg l(-1) ) for 48 h induced a substantial enhance in cell apoptosis, although pretreatment with ghrelin eradicated AGEs-induced apoptosis in HUVECs, as evaluated by MTT assays, flow cytometry and Hoechst 33258 staining. The induction of caspase-3 activation was also prevented by ghrelin in cells incubated with AGEs. Coverage to ghrelin (ten(-6) M) resulted inside a speedy activation of extracellular signal-regulated protein kinase (ERK)1/2 and Akt. The inhibitory impact of ghrelin on caspase-3 exercise was attenuated by inhibitors of ERK1/2 (PD98059), PI3K/Akt (LY294002) and growth hormone secretagogue receptor (GHSR)-1a (D-Lys(three) -growth hormone releasing peptide-6). The outcomes of this review indicated that ghrelin could inhibit AGEs-mediated cell apoptosis by way of the ERK1/2 and PI3K/Akt pathways and GHSR-1a was also concerned in the protective action of ghrelin in HUVECs. As such, ghrelin demonstrates substantial potential for preventing diabetic cardiovascular issues.