Abstract
The objective of our work was to investigate the influence of Fasudil, a Rho inhibitor on the number and function of the late endothelial progenitor cells in peripheral blood of chronic obstructive pulmonary diseases (COPD) patients with pulmonary artery hypertension. Eighty COPD patients with pulmonary artery hypertension were selected and divided into two groups: the treatment group and the control group, which had 40 patients respectively. The control group received routine treatment, including oxygen uptake, anti-infection and phlegm dissolving. The treatment group received the Fasudil in addition to the routine treatment. The changes on the number and function of the late endothelial progenitor cells in peripheral blood of the patients before and after the treatment were compared between the two groups. The changes on the pulmonary artery pressure were also compared. The number of the late endothelial progenitor cells in peripheral blood of the treatment group increased and the function was enhanced. The pulmonary artery pressure was reduced. The difference before and after the treatment and with the control group was statistically significant (p<0.05). The changes on the number and function of the late endothelial progenitor cells in peripheral blood and the pulmonary artery pressure before and after the treatment of the control group were not statistically significant (p>0.05). The Rho-kinase inhibitor Fasudil increased the number and enhanced the function of the late endothelial progenitor cells in peripheral blood of COPD patients with pulmonary artery hypertension.
Highlights
Hypoxic pulmonary artery hypertension (PAH) is the core stage of the pathogenesis process of chronic obstructive pulmonary diseases (COPD)
Studies in recent years demonstrated that the damage and malfunction of endothelium play an important role in the pathogenesis and development of PAH [ ]
Late endothelial progenitor cells (EPC) Identification The late EPC cultured in isolation was measured for the positivity of cell phenotypes of CD and KDR by a flow cytometry (Figure ) and the absorption of DiLDL combining with FITC-UEA-I (Figure )
Summary
Hypoxic pulmonary artery hypertension (PAH) is the core stage of the pathogenesis process of chronic obstructive pulmonary diseases (COPD). The decrease of the pulmonary artery pressure retards the pathogenesis and development of COPD significantly [ ]. Submitted: 8 September 2013 / Accepted: 6 February 2014 to decrease the pulmonary artery pressure is the key to prevent and cure COPD and cor pulmonate. Studies in recent years demonstrated that the damage and malfunction of endothelium play an important role in the pathogenesis and development of PAH [ ]. Following research considered the late EPC, coming from the bone marrow, as the real EPC, which directly takes part in the repairment of vascular endothelium and plays an important role in the neogenesis and repairment of blood vessels [ ]. The relationship between Rho/Rho-kinase signaling pathway and cardiopulmonary vascular diseases has drawn
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