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Objective. To investigate the effects of emodin on nitric oxide (NO) secretion induced by high glucose in human umbilical vein endothelial cells (HUVECs) through the p-Akt signaling pathway. Methods. Sensitivity of cells to emodin was determined by MTT assay to establish the experimental concentrations; then, HUVECs were treated with high-dose (33.3 mmol/L) glucose (HG), HG + emodin (HG + E), HG + the Akt phosphorylation inhibitor LY294002 (HG + LY), or HG + E + LY. The p-Akt (Ser 473) expression in 48 h was analyzed using Western blot. NO effect on the secretion of HUVECs was analyzed using nitrate reductase assay. Results. The sensitive emodin concentration for HUVECs growth was 10 mol/L (P<0.05). Compared with the HG group, NO secretion was significantly higher in the HG + E group (P<0.05), whereas it was lowest in the HG + LY group (P<0.05). Compared with the HG + LY group, NO secretion was increased in the HG + E + LY group (P<0.05). The p-Akt protein expression was decreased in the HG + LY group when compared to the HG group (P<0.05), while it significantly increased in the HG + E group (P<0.05). Compared with HG + LY group, p-Akt protein expression was significantly higher in the HG + E + LY group (P<0.05). Conclusion. Emodin could improve the NO secretion of HUVECs by high glucose through the p-Akt signaling pathway.

The Effect and Mechanism of Emodin on the NO Secretion of Human Umbilical Vein Endothelial Cells (HUVECs) Induced by High Glucose