Ghrelin combined with sodium tanshinone IIA sulfonate pretreatment reduces apoptosis and fractalkine expression induced by high-dose glucose in human umbilical vein endothelial cells.

BACKGROUND: To explore the regulatory role of ghrelin combined with sodium tanshinone IIA sulfonate (STS) pretreatment in cell apoptosis and fractalkine (FKN) expression of human umbilical vein endothelial cells (HUVECs) induced with high-dose glucose. METHODS: HUVECs were assigned into control group, high-dose glucose group (HG group), high-dose glucose with ghrelin group (Gr+HG group), and high-dose glucose companied with ghrelin and STS group (Gr+STS+HG group). The apoptosis of HUVECs was determined by Hoechst 33258 straining and flow cytometry (FCM). Nitric oxide (NO) level was measured by total NO assay kit. The mRNA and protein levels of beta-catenin, p-GSK-3beta and FKN were accessed by Western blot and real-time quantitative polymerase chain reaction (RT-qPCR), respectively. RESULTS: High-dose glucose significantly accelerated apoptosis in HUVECs. The apoptotic rate was lower in Gr+HG group and much lower in Gr+STS+HG group than control group. NO level was significantly reduced in the HG group, which was partly inhibited in Gr+HG group and obviously increased in Gr+STS+HG group than controls. In addition, mRNA levels of GSK-3beta and FKN in HUVECs decreased in Gr+HG group, which was more obviously decreased in Gr+STS+HG group. However, ghrelin treatment upregulated beta-catenin and p-GSK-3beta (Ser9), but downregulated FKN during high-dose glucose treatment, which was more obvious in Gr+STS+HG group. CONCLUSIONS: Pretreatment of ghrelin combined with STS reduces the apoptosis rate of HUVECs induced by high glucose environment and inhibits the expression of FKN via beta-catenin/Wnt signaling pathway.