1.The influence of hyperbaric oxygen therapy started at different time on patients with acute cerebral infarction
Aiqiong FENG ; Shaoxia ZENG ; Lihong QIN
Chinese Journal of Primary Medicine and Pharmacy 2005;0(02):-
Objective To study the influence of different starting time of hyperbaric oxygen(HBO) therapy on severe brain injury patients.Methods 60 cases of acute cerebral infarction patients were divided into 2 groups,namel 48 hours to 7 days group(group A) and 8 days to 15 days group(group B) after injury.Fugl-Meyer assemment and modified Barthel index were employed to assess the patients before and after HBO for 30 days in the 2 groups.Results After 30 days of HBO therapy the Fug-Meyer assemment and modified Barthel index in the A group were better than those of B group,there were significant differences between the 2 groups(P
2.Hypertension activates vessel wall oxygen and metabolism sensing pathways and accelerates atherosclerosis
Weidong JANG ; Aiqiong QIN ; Yusheng LIU ; Xin WANG ; Qinghua LU ; Zhiming GE
Chinese Journal of Geriatrics 2012;(12):1103-1107
Objective To study the molecular mechanism of atherosclerosis induced by intravascular pressure.Methods Technic aortic coarctation (TAC) was performed in ApoE-/-mice (n=8) and control littermate (n=8) mice.HE staining was performed in the vessels upstream and downstream of the mice models.In vitro,hypoxia inducible factor-1a (HIF-1α),heme oxygenase,reactive oxygen species and phosphorylated AMP activated protein kinase (AMPK) were analyzed in different intravascular pressure with a myograph system that allowed independent variation of flow and pressure.Results After one month of TAC,ApoE/ mice in a normal chow diet developed occlusive plaque and accelerated atherosclerotic lesions exclusively in upstream high-pressure vessel segments.In vitro,HIF-1α was increased,heme oxygenase was higher over(2.7 ±0.6) fold,reactive oxygen species and phosphorylated AMPK were also enhanced in high intravascular pressure perfused vessel segments as compared with low intravascular pressure perfused vessel segments (all P<0.05).Conclusions Intravascular pressure elevation can activate hypoxia and metabolism-associated pathways in the arterial wall,and predispose atherosclerosis accelerated.
3.Relationship between epidermal growth factor-like domain 7 and angiogenesis in atherosclerotic plaques
Weidong JIANG ; Jiping ZENG ; Yusheng LIU ; Xin WANG ; Aiqiong QIN ; Qinghua LU ; Zhiming GE
Chinese Journal of Geriatrics 2012;31(1):39-43
Objective To evaluate the expression of epidermal growth factor-like domain 7 (Egfl7) in atherosclerotic plaques and effects of its small interference RNA (siRNA) on angiogenesis gene expression in human endothelial cell line (HUVEC). MethodsEgfl7 expression in atheroscleroticplaquesweredetectedinhumaniliacarteryandmousearteriaeusing immunohistochemistry and immunofluorescence stainings.The siRNA targeting Egfl7 was transfected into HUVEC by lipofectamine with non-transfected cells and unconcerned siRNA as controls.At 0 h,12 h,24 h and 48 h after intervention,the levels of mRNA and protein of Egf17,vascular endothelial growth factor(VEGF),platelet derived growth factor-A (PDGF-A),platelet derived growth factor-B (PDGF-B),vascular cell adhesion molecule(VCAM) and intercellular adhesion molecule (ICAM)were measured by RT-PCR and Western blotting,respectively. ResultsThe expressions of Egfl7 in human iliac artery and mouse arteriae were increased.The expressions of Egfl7 in HUVEC at the levels of mRNA were[(0.14±0.02),(0.09±0.01),(0.02±0.01)]and the levels of protein[(0.71±0.11),(0.39±0.09),(0.07±0.01)]at 12 h,24 h and 48 h after siRNA intervention,respectively,which were decreased as compared with 0 h intervention [(0.31 ±0.05) and (0.93±0.08) ].Other genes such as VEGF,PDGF-A and PDGF-B were reduced or silenced at the levels of protein and mRNA in HUVEC with siRNA longer interventions(all P<0.05).ConclusionsThe expression of Egfl7 in atherosclerotic plaques is increased.The siRNA inhibiting Egfl7 gene expression results in silence of other factors involved in angiogenesis.