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. 2017 Oct 9;16(6):8635–8642. doi: 10.3892/mmr.2017.7740

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Copyright: © Zhou et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 6. — HG (35 mmol/l) increased the mRNA levels of VEGF, VEGFR-2, endocan in a time-dependent manner from 12 to 48 h. However, the growth trend began to slow down in 72 h. 100 µmol/l CaD prevented the increase of VEGF, VEGFR-2 and endocan levels induced by HG. HG also increased the mRNA levels of ICAM, MCP-1 and PTX3 in a time-dependent manner from 12 to 72 h. 100 µmol/l CaD prevented the increase the expression of these inflammatory factors induced by HG. (A) HUVECs were incubated with control or experimental medium for 12 h. (B) HUVECs were incubated with control or experimental medium for 24 h. (C) HUVECs were incubated with control or experimental medium for 48 h. (D) HUVECs were incubated with control or experimental medium for 72 h. *P<0.05 vs. respective control or respective mannitol, HG+CaD, CaD group. HG, high glucose; VEGF, vascular endothelial growth factor; VEGFR, vascular endothelial growth factor receptor; ICAM, intercellular adhesion molecule; MCP-1, monocyte chemotactic protein 1; PTX3, pentraxin 3; CaD, calcium dobesilate; HUVECs, human umbilical vein endothelial cells.