检索结果-南通市图书馆

Hemostatic mechanism of the effect of Jianpi Yiqi Shexue decoction on vascular factors in immune thrombocytopenia model mice

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Journal of Traditional Chinese Medical Sciences 2022年第2期9卷 160-165页

作者： Ruibai Li Wei Ma Haiyan Lang Hao He Liyuan Lv Yayue Zhang Xinyi Chen Li Hou Department of Oncology and Hematology Dongzhimen HospitalBeijing University of Chinese MedicineBeijing100700China School of Pharmacy Xi'an Medical UniversityShaanxi ProvinceXi'an710021China

Objective: To explore the hemostatic mechanism of Jianpi Yiqi Shexue decoction(JYSD) by regulating vascular factors in an immune thrombocytopenia(ITP) mouse model.Methods: An ITP mouse model was established by the passive-immune modeling method, and interventional drugs used were prednisone tablets and JYSD. The platelet count;vascular activity-related factors v WF, VCAM-1, and TM;and VEGF and b FGF were used as observational indicators.Results: On the 8th day of administration, compared with the model group, platelet counts in the prednisone and JYSD groups increased(both P 1). Compared with the control group, the levels of v WF, VCAM-1, and TM in the other groups were lower(all P 1 level in the JYSD group was higher than that in the prednisone group(P =.012), but without significant difference compared with the model group(P =.051). The TM level in the JYSD group was the lowest(vs. the model group,P =.047;vs. the prednisone group, P =.006). Compared with the control group, the IOD values of VEGF and b FGF in the other three groups were lower(all P 1). The IOD values of VEGF in the prednisone and JYSD groups were both higher than those in the model group(P =.002 and P 1, respectively). The IOD values of b FGF among the model, prednisone, and JYSD groups were not statistically significant(P >.05).Conclusion: A vascular factor disorder is involved in the pathogenesis of ITP. JYSD can increase the platelet count, upregulate VEGF expression, and reduce the TM level. JYSD has the same effect as prednisone tablets in regulating platelet, v WF, VEGF, and b FGF, with a stronger effect in normalizing VCAM-1 and TM levels. The hemostatic mechanism of JYSD is closely related to the effective balance of vascular factors.

关键词： Jianpi Yiqi Shexue decoction von Willebrand factor vascular cell adhesion molecule-1 Thrombomodulin vascular endothelial growth factor Basic fibroblast growth factor

Neuroprotective effect of ONO-1078, a leukotriene receptor antagonist, on transient global cerebral ischemia in rats

在线全文

学校读者我要写书评

暂无评论

Acta Pharmacologica Sinica 2003年第12期24卷 67-73页

作者： ZHANG Li-Hui~(2,3), WEI Er-Qing~(2,4) ~2Department of Pharmacology, School of Medicine, Zhejiang University, Hangzhou 310031 ~3Medical School, Hangzhou Teachers College, Hangzhou 310012, China Department of Pharmacology School of Medicine Zhejiang University Hangzhou 310031

AIM: To determine whether ONO-1078 {pranlukast, 4-oxo-8-[p-(4-phenylbutyloxy)benzoyl-amono]-2-(tetrazol-5-yl)-4H-1-benzopyran hemihydrate}, a potent leukotriene receptor antagonist, possesses a neuroprotective effect on global cerebral ischemia in rats, and to explore its possible mechanism of action. METHODS: Transient global cerebral ischemia was induced by four-vessel occlusion for 10 min and followed by 72-h reperfusion. ONO-1078 (0.03-0.3 mg/kg) and edaravone (MCI-186, 3-methyl-1-phenyl-2-pyrazolin-5-one, a neuroprotective agent) 10 mg/kg were ip injected 30 min before ischemia and 1 h after reperfusion, and once a day afterward. Neurological outcome was evaluated before ischemia and 24, 48, 72 h after reperfusion. Neuron density, the expressions of N-methyl-Daspartate (NMDA) receptor subunit proteins (NR1, NR2A, NA2B) and vascular cell adhesion molecule 1(VCAM-1) in the cerebral cortex and hippocampus were measured at 72 h after reperfusion. RESULTS: ONO-1078 (0.1, 0.3 mg/kg) and edaravone (10 mg/

关键词： ONO-1078 brain ischemia leukotriene antagonists neuroprotective agents N-methyl-D-aspartate receptors vascular cell adhesion molecule-1

Levels of soluble adhesion molecules in patients with various clinical presentations of coronary atherosclerosis

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Chinese Medical Journal 2010年第21期123卷 3123-3126页

作者： LU Hui-he SHENG Zheng-qiang WANG Yi ZHANG Li Department of Cardiology The Second Affiliated Hospital Nan Tong University Nantong Jiangsu 226601 China

Background adhesion molecules play an important role in the development and progression of coronary atherosclerosis. The aim of this study was to compare concentrations of soluble forms of adhesion molecules in patients with different clinical presentations of coronary artery disease （CAD）.Methods One hundred and twenty-eight patients with CAD were divided into three groups; the first group was acute myocardial infarction group （AMI group, n=45）, the second group was unstable angina pectoris group （UAP group, n=48）,the third group was stable angina pectoris group （SAP group, n=35）. We compared them with patients with normal coronary arteries （control group, n=31）. The serum levels of vascular cell adhesion molecule （VCAM-1）, intercellular adhesion molecule-1 （ICAM-1）, E-selectin and P-selectin were measured in all subjects.Results The serum level of VCAM-1 in the AMI group was significantly higher than in the UAP, SAP and control groups （P 〈0.01）. The level in the UAP group was significantly higher than the SAP group and control group （P 〈0.01） and the level in the SAP group was significantly higher than in the control group （P 〈0.01）. The serum ICAM-1 level was significantly elevated in the AMI, UAP and SAP groups as compared to the control group （P 〈0.01）. The levels of serum E-selectin and P-selectin in the AMI and UAP groups were significantly higher than in the SAP and control groups （P〈0.01）.Conclusions Increased levels of VCAM-1 and ICAM-1, E-selectin and P-selectin, as markers of inflammation, showed the importance of inflammatory processes in the development of atherosclerosis and clinical expression of CAD. Soluble ICAM-1, VCAM-1, E-selectin and P-selectin concentrations are useful indicators of the presence of atherosclerosis and the severity of CAD clinical presentation.

关键词： vascular cell adhesion molecule-1 intercellular adhesion molecule-1 E-selectin P-selectin coronary artery disease inflammation

Pingyangmycin-regulated Expressions of adhesion molecules in Human Venous Malformation Endothelial cells

在线全文

学校读者我要写书评

暂无评论

Journal of Huazhong University of Science and Technology(Medical Sciences) 2012年第5期32卷 760-766页

作者：贾玉林贾俊赵怡芳 Department of Oral and Maxillofacial Surgery Union HospitalTongji Medical CollegeHuazhong University of Science and Technology Department of Oral and Maxillofacial Surgery College & Hospital of StomatologyWuhan University

Pingyangmycin (bleomycin A5 hydrochloride,PYM) is one of the anti-neoplastic agents which have been commonly used to treat venous malformations.However,the underlying mechanism by which PYM treats venous malformations remains poorly understood.It was reported that venous endothelial cells could recruit neutrophils via adhesion molecules (E-selectin,ICAM-1,ICAM-3,VCAM-1) during the acute/chronic inflammation and subsequent histological fibrosis after sclerotherapy with PYM.This study explored if the expression of E-selectin,ICAM-1,ICAM-3 and VCAM-1 in human venous malformation endothelial cells could be affected by PYM.HVMECs were cultured from human venous malformation tissue.Expressions of E-selectin,ICAM-1,ICAM-3 and VCAM-1 on HVMECs in response to PYM were analyzed by cell ELISA.The relative levels of mRNA expression in the cells were semi-quantified.The results showed that PYM up-regulated the expressions of E-selectin,ICAM-3,VCAM-1 and ICAM-1 in both time-and concentration-dependent manner.Our findings suggested that PYM could induce the expression of adhesion molecules in HVMECs,which might be a possible mechanism by which sclerotherapy by intralesional injection of PYM treats venous malformations.

关键词： E-selectin intercellular adhesion molecule-1 intercellular adhesion molecule-3 vascular cell adhesion molecule-1 cell culture

Involvement of Activation of C-Met Signaling Pathway in CD151-induced HUVECs Angiogenesis

在线全文

学校读者我要写书评

暂无评论

Journal of Huazhong University of Science and Technology(Medical Sciences) 2015年第1期35卷 35-41页

作者：汤清辉刘曌宇左后娟刘正湘 Department of Cardiology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Department of Gastroenterology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology

CD151 is a member of the tetraspanin family that is implicated as a promoter of pathological or physiological angiogenesis. C-Met is expressed on a variety of cells including vascular endothelial cells（VECs） and up-regulated during angiogenesis. In this study, we investigated whether CD151 regulated migration, proliferation, tube formation and angiogenesis of human umbilical VECs（HUVECs） with activation of C-Met. Moreover, we studied whether CD151 could affect the angiogenic molecules such as nitric oxide（NO）, vascular cell adhesion molecule-1（VCAM-1） and vascular endothelial growth factor（VEGF）. The expression of CD151 was determined by Western blotting. The cell proliferation assay was performed using the cell counting kit-8（CCK-8） method and cell migration was assessed in microchemotaxis chambers by using fetal bovine serum（FBS） as the chemotactic stimulus. The angiogenic molecules were evaluated using ELISA. The NO level was detected using NO detection kit. The potential involvement of various signaling pathways was explored using relevant antibodies. We found that proliferation, migration and tube formation of HUVECs were promoted by CD151 with activation of C-Met, FAK and CDC42, while they were suppressed with CD151 knockdown by RNAi. Similarly, the levels of NO, VCAM-1 and VEGF in HUVECs were increased by CD151, but they were inhibited with CD151 knockdown by RNAi. These data suggested that CD151 could promote migration, proliferation, tube formation and angiogenesis of HUVECs, which was possibly related to the C-Met signaling pathways.

关键词： CD151 C-Met vascular endothelial growth factor vascular cell adhesion molecule-1 angiogenesis

Study on the action of resistin-induced human umbilical vein endothelial cell dysfunction

在线全文

学校读者我要写书评

暂无评论

Frontiers of Medicine 2007年第2期1卷 196-199页

作者： LI Zhizhen LI Fangping YAN Li LI Feng LI Yan CHENG Hua FU Zuzhi Department of Endocrinology Second Affiliated HospitalSun Yat-Sen UniversityGuangzhou 510120China

The aim of this paper was to investigate the effects of resistin on human umbilical vein endothelial cells(HUVECs),and to explore its role and mechanism of action in atherosclerosis.HUVECs were incubated with recombinant human resistin(0,50,100 ng/mL)for 24 h.ICAM-1,VCAM-1 and reactive oxygen species(ROS)were assayed by flow cytometer.ET-1,eNOS and iNOS mRNA expression were measured by semi-quantitative RT-PCR.Incubation of HUVECs with resistin resulted in an increase in ICAM-1 expression and ET-1 mRNA expression.However,resistin had no effect on VCAM-1 expression and ROS release.eNOS and iNOS mRNA expression were not altered by resistin stimulation.Adipokine resistin exerted a direct effect in promoting HUVEC dysfunction by promoting ICAM-1 and ET-1 expression.These data suggest that adipocyteendothelium cross-talk might play an important role in the pathogenesis of cardiovascular disease in diabetes mellitus.

关键词： resistin umbilical veins endothelial cells intercellular adhesion molecule-1 vascular cell adhesion molecule-1

Effect of hyperlipidemia on endothelial VCAM-1 expression and the protective role of fenofibrate

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Frontiers of Medicine 2007年第4期1卷 356-358页

作者： WU Jun LIN Jinchao HE Zhaochu OU Biru GUO Haisen Department of Cardiology First Affiliated Hospital of Guangzhou Medical CollegeGuangzhou 510120China

The effect of hyperlipidemia and inflammation on endothelial functions was studied.The enrolled included control(basic chow),hyperlipidemia and fenofibrate-treated groups(high fat diet).The hyperlipidemia model was set up by four-week atherogenic diet,followed by a 16-week treat-ment in the fenofibrate-treated group(fenofibrate 40 mg/kg every day)and without treatment in the hyperlipidemia group,respectively.In the 20th week,serum lipid level and NO levels were measured,and the expression of vascular cell adhesion molecule-1(VCAM-1)and cell adhesiveness in aortic endothelia observed by computer-aided ***-pared with the control group,hyperlipidemia rats showed lower levels of NO and increases in leukocyte accumulation on the endothelial surface,also stronger and more extensive endothelial expression of VCAM-1.In fenofibrate-treated group,the expression of VCAM-1 and leukocyte accumula-tion on the endothelial surface was decreased,while serum levels of NO were increased as compared with hyperlipidemia group.Hyperlipidemia can inhibit the NO activity and pro-mote the damage of VACA-1 to aortic endothelia.Fenofibrate can effectively prevent the pathogenesis of atherosclerosis by restoring NO levels and down-regulating the VCAM-1 expression.

关键词： hyperlipidemias vascular cell adhesion molecule-1 nitric oxide fenofibrate

Acupuncture for cerebral ischemia/reperfusion injury Does it reduce the inflammatory reaction?

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Neural Regeneration Research 2010年第14期5卷 1055-1060页

作者： Zhenyan Li Guangwei Zhong Sujuan Huang Yunsheng Liu Sue Wang Wei Li Department of Neurosurgery Xiangya Hospital Central South University Changsha 410008 Hunan Province China Institute of Integrated Traditional and Westem Medicine Xiangya Hospital Central South University Changsha 410008 Hunan Province China Operating Room Xiangya Hospital Central South University Changsha 410008 Hunan Province China

BACKGROUND： Nuclear factor-κB （NF-κB）, intercellular adhesion molecule-1 （ICAM-1）, and vascular cell adhesion molecule-1 （VCAM-1） in brain tissue can participate in inflammatory reactions after cerebral ischemia. Acupuncture treatment for acute cerebral ischemia produces abnormal protein expression. OBJECTIVE： To investigate the effects of acupuncture on NF-KB, ICAM-1, and VCAM-1 mRNA and protein expression in the brain tissue of rats with cerebral ischemiaJreperfUsion injury. DESIGN, TIME AND SETTING： Randomized, controlled, animal experiments were performed at the Laboratory of Department of Neurosurgery, Xiangya Hospital, Central South University, China between December 2008 and October 2009. MATERIALS： Rabbit anti-NF-KB polyclonal antibody, rabbit anti-ICAM-1 polyclonal antibody, and rabbit anti-VCAM-1 polyclonal antibody were purchased from Santa Cruz Biotechnology, USA. METHODS： A total of 46 healthy, Sprague Dawley rats were randomly assigned to sham surgery （n= 10）, model （n = 12）, acupuncture pretreatment （n = 12）, and acupuncture intervention （n = 12） groups. Models of middle cerebral artery occlusion were established by right common carotid artery ligation. In the acupuncture pretreatment group, rats received acupuncture for 3 consecutive days, and then models were established. In the acupuncture intervention group, rats received acupuncture for 3 consecutive days at Waiguan （SJ 5）, Sanyinjiao （SP 6）, and Dazhui （DU 14） acupoints following model establishment. MAIN OUTCOME MEASURES： Somatosensory asymmetry and forelimb use asymmetry were tested, as well as NF-KB, ICAM-1, and VCAM-1 mRNA and protein expression in the frontal and parietal cortex at 4, 12, 24, 48 and 72 hours following cerebral ischemia/reperfusion injury. RESULTS： Acupuncture improved neurological function and significantly decreased NF-KB, ICAM-1, and VCAM-1 mRNA and protein expression in the frontal and parietal cortex of rats with cerebral ischemia/reperfusion injury （P 〈 0.05）. CONCLUSION： Acupuncture can improve neurological functio

关键词： cerebral ischemia/reperfusion nuclear factor-κB, intercellular adhesion molecule-1 vascular cell adhesion molecule-1 acupuncture traditional Chinese medicine neural regeneration

Sphingosine Kinase/Sphingosine 1-Phosphate(S1P)/S1P Receptor Axis is Involved in Liver Fibrosis-Associated Angiogenesis

在线全文

学校读者我要写书评

暂无评论

Sphingosine Kinase/Sphingosine 1-Phosphate(S1P)/S1P Receptor...