Objective:To investigate the protective mechanism of Xiaotan Huayu Likiao Formula(XHLF)in improving thoracic aortic endothelial cell injury in mice with chronic intermittent hypoxia(CIH).Methods:Twenty-four healthy male C57BL/6N mice aged 8 weeks were randomly divided into four groups:normoxia group(Con),chronic intermittent hypoxia exposure group(CIH),CIH+XHLF group,and Con+XHLF group.The CIH group and the CIH+XHLF group were exposed to an intermittent hypoxic environ-ment.The CIH+XHLF and Con+XHLF groups were administered XHLF daily by gastric lavage(26.8 g/kg/d),while the CIH and Con groups were given an equal volume of normal saline for a total of 28 days.The tail-cuff method was used to monitor the mouse blood pressure;HE and Masson staining to observe the pathological changes in the thoracic aorta;The serum levels of nitric oxide(NO)and vascular endothelial growth factor(VEGF)were measured.Mitochondrial morphology was observed under transmission electron micros-copy.TUNEL staining was used to detect apoptosis of thoracic aortic cells;Immunohistochemical staining to detect the expression of Cleaved Caspase-3,Bcl-2-associated X protein(Bax),and B-cell lymphoma-2 gene(Bcl-2)proteins.Results:Compared with the Con group,the systolic blood pressure of mice in the CIH group increased after 21 days(P＜0.05).The vascular intima was uneven,the nuclear arrangement was disordered,and the elastic fibers were reduced.The level of VEGF in the serum increased,while the level of NO decreased(P＜0.05).Mitochondria showed shrinkage and cristae frac-ture.The apoptosis level increased,and the expressions of Cleaved Caspase-3 and Bax proteins were enhanced,while the expression of Bcl-2 protein was weakened(P＜0.05).Compared with the CIH group,the blood pressure of mice in the CIH+XHLF group decreased(P＜0.05),and vascular endothelial function and injury improved(P＜0.05).Vascular endothelial mitochondrial damage was im-proved,and the apoptosis level decreased(P＜0.05).Conclusion:XHLF may improve thoracic aortic vascular injury and dysfunction caused by CIH exposure by inhibiting apoptosis.
维普
万方数据
