Mechanism of Vascular Endothelial Injury and Repair in Intermittent Hypoxia Rat Model

WANG Yan; SHI Yao; FENG Jing; CAO Jie; CHEN Baoyuan

doi:10.3969/j.issn.1002-266X.2014.19.007

Abstract：Objective To explore the mechanism of vascular endothelial injury and repair in an intermittent hypoxia (IH) rat model.Methods 30 male Wistar rats were randomly divided to two groups according to the exposure conditions :(1) normal oxygen control group (IN group, n=15);(2) IH group (n=15).In 13~16 weeks, two groups were ex-posed to normal oxygen or IH, respectively.After exposure, ELISA method was used to detect value of tumor necrosis fac-tor alpha ( TNF-α) and interleukin ( IL)-6 in plasma and in the endothelium of right common carotid artery .Real-time-PCR assay was used to analyze RhoA mRNA level in the endothelium of right carotid artery .Flow cytometry was used to de-tect EPC level in peripheral blood .We also obtained a piece of tissue of right carotid artery , then performed paraffin em-bedding, sectioning, HE staining, and observed in light microscope for counting the percentage of intima-media thickness (IMT) in the all wall (C-IMT%) by means of Photoshop software .Results IH group had higher TNF-α(48.59 ±3.20 vs 16.47 ±2.25 pg/mL in plasma;112.90 ±13.91 vs 37.60 ±3.98 pg/mL in endothelial cell), IL-6 (264.57 ±16.69 vs 109.71 ±7.84 pg/mL in plasma;675.30 ±15.01 vs 434.60 ±16.05pg/mL in endothelial cell), RhoA mRNA (1.56 ± 0.05 vs 1.00 ±0.00) and C-IMT%(0.534 ±0.02 vs 0.488 ±0.013) than IN group (all P<0.05).The elasticity of vessel decreased , and hardness increased in IH group , that occurred inflammatory injury .The quantity of endothelial pro-genitor cell (EPC) were higher in IN group than IH group (8.89 ±0.59 vs 5.85 ±0.43个/μL, P<0.05).Conclusion IH damaged vascular endothelium in rat , activated the inflammation pathway of TNF-α, IL-6 and RhoA , increased endo-thelial cell premeability and systematic inflammation .At the same time, IH reduced the quantity of EPC both in peripheral blood and in the damage region , as a result the repair capacity for endothelium reduced , which increased the risk of cardio-vascular diseases .