Protective effects of monosialotetrahexosylganglioside sodium on H2O2-induced human vascular endothelial cells.

Monosialotetrahexosylganglioside sodium (GM1) is widely used in the treatment of central and peripheral neurological injuries. In addition to its neuroprotective activity, GM1 exerts protective effects on brain microvascular endothelial cells, although the mechanisms underlying these effects remain unclear. The aim of the present study was to clarify the protective effects and underlying mechanisms of GM1 on human umbilical vein endothelial cells (HUVECs). In this study, hydrogen peroxide (H2O2) was applied to induce the HUVEC injury. HUVECs in a logarithmic growth phase were divided into five groups, namely the control, H2O2-treated, 10-mg/l GM1, 5-mg/l GM1 and 1-mg/l GM1 groups. In all the groups, cell proliferation was detected using a Cell Counting Kit-8 assay, a flow cytometric method was applied to analyze the cell cycle and nuclear factor (NF)-κB expression was evaluated using immunofluorescence analysis. In addition, the protein expression levels of NF-κB, phosphatidylinositol 3-kinase (PI3K) and glycogen synthase kinase (GSK)-3 were detected via western blot analysis. The results indicated that GM1 exerted significant protective effects on H2O2-injured cells by increasing the ratio of cells in the S/G2 phase. Furthermore, western blot analysis revealed that PI3K expression levels were markedly increased after 24 h, as a result of the GM1 treatment, while the expression of both GSK-3 markedly decreased. In addition, the ratio of nuclear-to-cytoplasmic NF-κB expression increased in the GM1-treated cells. In summary, GM1 exhibited marked protective effects on the HUVECs, possibly due to the ability of GM1 in maintaining the integrity of the endothelium and increasing the proportion of cells undergoing mitosis, a process in which the PI3K/GSK-3 and NF-κB pathways are crucially involved.