Abstract: Objective To explore the important role of neutrophil (PMN) and vascular endothelial cell (VEC) interaction in vascular endothelial injury induced by overlap syndrome and the relationship with the action of intercellular adhesion molecule (ICAM)-1 at the cellular level. Methods Samples of fasting peripheral venous blood were taken from 16 healthy volunteers, 2.5 mL per person, 40 mL were sampoed at each time and 10 times were sampoed successively. PMN was separated by double-layer density gradient centrifugation. Then the experimental group directly co-cultured with neutrophils and endothelial cells was placed in the cell culture incubator simultaneously with the control group of endothelial cells alone.The culture was carried out for 4 hours, and then the respiratory simulation system of the Department of Respiratory Medicine of Tianjin Medical University General Hospital was used for intermittent and continuous hypoxia exposure for 8 hours. After exposure, the supernatant and endothelial cells were collected separately. The inflammatory factors in the supernatant including interleukin (IL) - 6, tumor necrosis factor (TNF) - α, adhesion molecule ICAM-1, catalase (CAT)activity and malondialdehyde (MDA) concentration were detected. The expression levels of VEC pro-apoptotic gene Bak and anti-apoptotic gene Bcl-xl mRNA were detected by qRT-PCR. Results The concentrations of IL-6, TNF-α, ICAM-1 and MDA were significantly higher in the experimental group than those in the control group (P＜0.05). The activity of CAT was significantly lower in the experimental group than that in the control group (P＜0.05). The expression levels of Bak mRNA and Bcl-xl mRNA were significantly higher in the experimental group than those in the control group, while Bcl-xl/Bak was significantly lower than that in the control group (P＜0.05). In experimental group ICAM-1 was positively correlated with IL-6, TNF - α and MDA, but ICAM-1 was negatively correlated with CAT and Bcl-xl / BAK (P＜0.05). Conclusion The interaction between PMN and VEC aggravates vascular endothelial injury caused by overlap syndrome, and ICAM-1 plays an important role in it.

Key words: vascular system injuries, intercellular adhesion molecule-1, inflammation, oxidative stress, apoptosis, cell interaction；overlap syndrome