Effects of Tricalcium Silicate Cement on Corneal Cell Proliferation and Its Relationship with Vascular Endothelial Growth Factor Level and Receptor Typing

This research analyzed the effects of tricalcium silicate (C3S) cement and hypoxia on proliferation of human corneal epithelial cells (HCEpiCs) and the levels of vascular endothelial growth factor (VEGF) and its receptors (VEGFRs). Nanoscale C 3 S was prepared using a combustion method and characterized using X-ray diffraction (XRD), scanning electron microscopy (SEM), and laser particle size (LPS) analyzer. HCEpiCs were cultured, and influences of C 3 S with changed concentrations on proliferation of (HCEpiCs were analyzed. The cells were treated with hypoxia or with low-concentration (0.5 mg/mL, LC-C 3 S), medium-concentration (5 mg/mL, MC-C 3 S), or high-concentration (50 mg/mL, HC-C 3 S) of C 3 S. Meanwhile, normal HCEpiCs were undertaken as controls (Ctrl group). Cell proliferation, apoptosis, and the expression of target genes were detected using CCK-8, Annexin V-FITC/PI, fluorescent quantitative polymerase chain reaction (fqPCR), and Western blotting (WB). The results suggested that nanoscale C 3 S had multiple morphologies and an average particle size (APS) of (231.5±8.3) nm. With increasing nanoscale C 3 S concentration, proliferation of HCEpiCs increased ( P < 0.05), and the highest proliferation was visualized at 5 mg/mL. Based on the conditions in the Ctrl group, the hypoxia group exhibited a decreased proliferation rate (PR), an increased apoptosis rate (AR), downshifted VEGF, VEGFR-2, and VEGFR-3, and elevated VEGFR-1 ( P < 0.05). Based on the hypoxia group, the LCC 3 S, MC-C 3 S, and HC-C 3 S groups presented increased cell PRs, decreased APs, upshifted VEGF, VEGFR-2, and VEGFR-3, and downregulated VEGFR-1 ( P < 0.05). The MC-C 3 S group showed an increased cell PR, a decreased AP, upregulated VEGF, VEGFR-2, and VEGFR-3, and downregulated VEGFR-1 to the LC-C 3 S group ( P < 0.05). Additionally, the HC-C 3 S group had a decreased cell PR, an increased AP, upregulated VEGF, VEGFR-2, and VEGFR-3, and a downshifted VEGFR-1 to the MC-C 3 S group ( P < 0.05). Therefore, C 3 S promoted proliferation of HCEpiCs, upregulated VEGF, VEGFR-2, and VEGFR-3, and downregulated VEGFR-1.