Abstract: Objective To investigate the characteristics of hypoxia model induced by cobalt chloride (CoCl₂) in human hepatic sinusoidal endothelial cells (HHSEC).Methods HHSEC were incubated with different concentrations of CoCl₂ (0～800 μM) for 24 h, in which cell viability was measured with counting kit-8 (CCK8) assay. Cell migration was detected by transwell assay after stimulating HHSEC with 50～200 μM CoCl₂. Matrigel lumen formation assay was used to detect cell lumen formation. Expressions of cell hypoxia inducible factor -1α (HIF-1α), von Willebrand factor (vWF) and vascular endothelial growth factor (VEGF) protein were detected by western blot. HIF-1α nuclear translocation was observed by immunofluorescence staining. Results Compared with control group, cell viability and cell migration of HHSEC were significantly increased, with a rich and airtight tubular structure formed in low concentration of 50～200 μM CoCl₂ group. Expressions of HIF-1α, vWF and VEGF in HHSEC were increased in 50 μM and 200 μM CoCl₂ group than those in the control group. Furthermore, expressions of HIF-1α and vWF in 200μM CoCl₂ group were higher than those in 50 μM CoCl₂ group.Conclusion Low levels of 50 μM and 200 μM CoCl₂ may induce HHSEC hypoxia and angiogenesis through promoting the expression and nuclear translocation of HIF-1α.

Key words: Cobalt chloride, Human hepatic sinusoidal endothelial cells, Hypoxia, Hypoxia-inducible factor-1α