Objective: To investigate the intervention effect of astragaloside on the expression of nuclear factor??(NF-?B) injured by hypoxia/reoxygenation(H/R) in vascular endothelial cells.Methods: The human umbilical vein endothelial cells(hUVECs) were cultured and passaged.After the third generation,hUVECs were randomly divided into three groups: control group,H/R group and astagaloside group.The cells in the control group were cultured under normal conditions;the cells of H/R group were cultured under hypoxia,in a closed container with oxygen concentrations below 1% for 1 hour,and then under normal conditions for 1 hour in a CO2 foster box;the hUVECs in astragaloside group were pretreated by different dose of astragaloside(the final concentrations of 20,40,80 mg/L) at the time of pre-hypoxia,after 12 hours of the pretreatment,they suffered from H/R.The concentration of intercellular adhesion molecule-1(ICAM-1) and content of malondialdehyde(MDA) in supernatant were detected respectively by ABCenzyme linked immunosorbent assay(ELISA) and thio-barbituric acid method.The expression of NF-?? of the vascular endothelial cells was analyzed by immunohistochemistry.Results: Compared with the control group,the content of MDA and concentration of ICAM1 in the supernatant fluid were remarkably increased in the H/R group(MDA content(6.98?1.15) ?mol/L vs.(2.38?0.49) ?mol/L,ICAM-1 concentration(3 169.01?132.75) ng/L vs.(995.14?74.93) ng/L,both P

AIM: To investigate the intervention effect of astragaloside on adhesion of polymorphonuclear neutrophils (PMN) and vascular endothelial cells and on expression of nuclear factor-?B (NF-?B) in human umbilical vein endothelial cells (hUVECs) injured by hypoxia/reoxygenation due to ischemia/reperfusion. METHODS: The experiment was performed at the Cell Bioengineering Laboratory of Institute of Cerebrovascular Diseases, Affiliated Hospital of Medical College, Qingdao University from September 2005 to May 2006. ①Neonatal umbilical cords were offered by Department of Gynecology and Obstetrics in Affiliated Hospital of Medical College of Qingdao University, with informed consent of puerperant and their families. The experiment was accorded with ethical standard of Helsinki declaration. ②The hUVECs were cultured to the future passage. After the third passage, hUVECs were randomly divided into three groups. Cells in a control group were cultured under normal conditions; Cells in a hypoxia/reoxygenation group were cultured under in closed container with hypoxia for 1 hour, and then under normal conditions for 1 hour; The hUVECs in a astragaloside group were pretreatment by different doses of astragaloside (20, 40, 80 mg/L). After 12 hours, hUVECs suffered from hypoxia/reoxygenation. ③The concentration of intercellular adhesion molecule (ICAM)-1 and content of malondialdehyde (MDA) in supernatant were detected by enzyme linked immunosorbent assay (ELISA) and thiobarbituric acid method. Expression of NF-?B of hUVECs was analyzed by immunohistochemistry. PMN adhesion to hUVECs was measured by rose Bengal staining. RESULTS: ①Compared to the control group, the content of MDA remarkably increased in hypoxia/reoxygenation group (P

Objective To investigate the molecular mechanisms of protective effects of thioredoxin (Trx) on human vascular endothelial cells in atherosclerosis.Methods The cell models of Trx-overexpressing cells (Ad Trx) and the control cells (Ad-con) were established by adenovirus vector gene transfer technology in human umbilical vein endothelial cells (HUVECs).The oxidized low density lipoprotein,a risk factor of atherosclerosis,was used as a stimulator.Western blot and indirect immunofluorescence were used to detect the protein expression levels and the cellular localization of Trx,adhesion molecules (ICAM-1,VCAM-1) and the upstream signal pathways.Trx activity was detected by insulin disulfide reduction assay,and cellular reactive oxygen species (ROS)production was detected by fluorescent probe DCFH-DA.Results As compared with control group,Trx protein expression level was enhanced in Ad-trx group and the Trx activity in Ad-Trx group was upregulated by (26.2 ±3.3)％.The result of ROS detection showed that overexpression of Trx significantly inhibited the cellular ROS generation.As compared with control group,overexpression of Trx obviously inhibited the adhesion molecules expression but markedly promoted the phosphorylation of Smad3 in endothelial cells with or without oxLDL stimulation (P＜0.05).Pretreatment of cells with SIS3,a specific inhibitor of Smad3 phosphorylation,reversed Trx-induced inhibition of adhesion molecules expression.Further studies showed that pretreatment of cells with SIS3 enhanced oxLDL-induced AP-1 subunit c-fos nuclear expression.Conclusions The enhancement of Smad3 phosphorylation and c-Fos nuclear expression are mainly responsible for the Trx-induced downregulation of adhesion molecules.

To investigate the effects of salvianolic acid B (SA-B) on cardiovascular endothelial cell function and platelet activation during myocardial ischemia-reperfusion in rabbits.

Objective To investigate the influencing factors on serum homocysteine level in healthy retired-elderly people in Tianjin,in order to provide theoretical basis and guidance for clinical intervention therapy.Methods A total of 184 participants meeting the standard of Chinese healthy elderly people (2013) were selected from 1247 retired-elderly people who took healthy physical examination in three grade Ⅲ-A hospitals in Tianjin from June to August in 2014.They were divided into two groups based on plasma Hcy level:hyper-homocystinemia group (≥15 μmol/L) and normal plasma Hcy level group (＜15μmol/L).The influencing factors on plasma Hcy level were analyzed by multiple stepwise regression and logistic regression analysis.Results The proportion of healthy retired-elderly people accounted for 14.76 ％,with men at 82.61％ and women at 17.39 ％,mean age (78.37±6.88) years.The Hcy level was higher in healthy males than in healthy females [(16.90± 6.86) μmol/L vs.(12.89 ± 5.97) μmol/L,P＜0.005].The proportion of people with hyper-homocystinemia accounted for 45.65％,and the mean Hcy concentration was (21.39±6.98) μmol/L.The age of people with hyper-homocystinemia was higher than that with normal Hcy [(80.58±6.09) years vs.(76.56±7.04) years,P＜0.005].There were no statistically significant differences in blood pressure,lipid and blood glucose levels and the proportion of patients with coronary heart disease,hypertension,type 2 diabetes mellitus,gout,periodontitis and other diseases between the two groups (all P＞0.05).Spearman correlation analysis showed that the level of serum Hcy was positively correlated with serum uric acid levels (P=0.000).Multiple stepwise regression and logistic regression analysis showed that age,gender and serum uric acid level were risk factors for plasma Hcy level in healthy elderly people.Conclusions Age,gender and serum uric acid level are risk factors for serum Hey level in healthy elderly people.

Objective To investigate the serum levels of brain derived neurotrophic factor (BDNF) and heat shock protein 70 (HSP70),and evaluate their clinical significance in brain injury of children with complicated febrile convulsions (CFC).Methods Forty-three patients with CFC,41 children with simple febrile convulsions and 36 healthy controls were recruited in this study; their serum levels of BDNF and HSP70 were detected by enzyme linked immunosorbent assay (ELISA); correlation between levels of BDNF and HSP70 and both time of twitch duration and twitch frequency were analyzed.Results The mean serum concentrations of BDNF (4.96±1.21 ng/mL) and HSP70 (2.86± 0.93 ng/mL) in patients of CFC group were significantly higher than those in patients of simple febrile convulsions and healthy controls (P＜0.05); while no significant difference was noted between patients of simple febrile convulsions and healthy controls (P＞0.05).These changes were closely related to the duration time and frequency of convulsions(r=0.553,P=0.015; r=0.587,P=0.012; r=0.526,P=0.024; r=0.562,P=0.018).Conclusions It is sure that some brain injury exists in children with CFC; BDNF and HSP-70 might be one of the molecular mechanisms for the brain injury and protective effect.