Effect of Naotaifang(脑泰方)Extract on Changes of Coagulation in Human Umbilical Cord Vein Endothelial Cell and Fibrinolysis Tumor Necrosis Factor-α

Objective:To observe the changes of coagulation and fibrinolysis function in human um-bilical cord vein endothelial cells(HUVEC)induced by recombinant human tumor necrosis factor-α(rhT-NF-α)and the effect of Naotaifang extract(脑泰方,NTE)on it.Methods:Cultured HUVEC is randomlydivided into six groups:Control group,NTE Control group(Only 2 g/L NTE),rh TNF-αgroup(100μg/L rhTNF-α),and low-dosage,middle-dosage and high-dosage NTE group(100μg/L rhTNF-αand 0.67g/L,2 g/L,6 g/L NTE).The coagulation activity of frozen-dissolved HUVEC,von Willebrand factor(vWF)content in the conditioned medium and tissue-type plasminogen activator(tPA)and plasminogenactivator inhibitor(PAI)activity were to be detected after 24 hrs.Results:Compared with the controlgroup,PAI activity were enhanced,vWF release markedly increased in conditioned medium of TNF-αgroup(P<0.01)and the frozen-dissolved HUVEC markedly shortens the rabbit plasma prothrombintime,and the above changes could be significantly inhibited by the 3 dosages o     

Effect of Tumor Necrosis Factor-αon Resistin Expression in 3T3-L1 Adipocytes and Its Mechanism

Insulin resistance plays an important role inthe pathogenesis, development and complication indiabetes mellitus. Obesity is one important cause,but its mechanism is complicated. Steppan foundthat resistin had direct effect on insulin in mouseadipose cells in 2001 and believed that it might bethe key molecule of diabetes mellitus[1]. TNFαis apolypeptide which has extensive biological actionand effects in the development of anti tumourmechanism, immunoloregulati…     

Effects of static magnetic field on human umbilical vessel endothelial cell

Objective： To investigate the effects of static magnetic field（SMF） on the viability, adhesion molecule expression of human umbilical vessel endothelial cell. Methods： Magnetic flux intensity was 0. 1 mT, 1 mT, 10 mT. Cell viability and proliferation were measured with ^3H-TdR and MTT methods; and apoptosis of human umbilical vein endothelial cell （HUVEC） was studied by flow cytometry and transmission electric microscopy. ELISA was used to measure the expression of ICAM-1 and VCAM-1 on endothelium. Results： 0.1 mT SMF had no effects on the growth of HUVEC, however, SMF of 1 mT, 10 mT attenuated growth of HUVEC. 10 mT static magnetic field could induce apoptosis and necrosis of HUVEC. 10 mT SMF enhanced the expression of ICAM-1 and VCAM-1 on endothelium. Conclusion： The effect of SMF depends on the intensity of SMF. 10 mT SMF has adverse effects on human umbilical vessel endothelial cell.     

Effects of angiotensin Ⅱ on human umbilical vein endothelial cells senescence and the telomerase activity

目的 观察血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)对人脐静脉内皮细胞(human umbilical vein endothelial cell,HUVECs)衰老的诱导作用及对端粒酶活性的影响.方法 体外培养HUVECs,采用CCK-8法检测细胞存活率,用AngⅡ(终浓度10-6 mol/L)干预,分为对照组和AngⅡ诱导组.β-半乳糖苷酶活性采用免疫化学染色方法,流式细胞术检测细胞周期来反映细胞的增殖能力;用聚合酶链反应-酶联免疫吸附法(PCR-ELISA)检测端粒酶活性.结果 与对照组比较,10-6 mol/L AngⅡ诱导组存活的细胞数为对照组的(77.15±6.83)%;(71.10±6.81)%的细胞呈现β-半乳糖苷酶阳性染色,流式细胞仪检测细胞周期多停滞于G0/G1期[(84.11±7.92)%],证实细胞衰老;与对照组相比,10-6 mol/L AngⅡ诱导组端粒酶活性明显下降(P<0.01).结论 AngⅡ可以诱导HUVECs衰老,其机制可能与抑制衰老细胞端粒酶活性有关.     

Cloning and expression of human arresten gene and effect of its recombinant protein on endothelial cell proliferation

Cloning and expression of human arresten gene and effect of its recombinant protein on endothelial cell proliferation@宋自芳$Dept Gener Surg,Union Hosp,Tongji Med Col,Huazhong Univ Sci Technol,Wuhan 430022     

Effect of Salvia Miltiorrhiza Bge on Left Ventricular Hypertrophy and the Expression of Tumor Necrosis Factor-α in Spontaneously Hypertensive Rats

The effects of salvia miltiorrhiza Bge (SMB) on left ventricular hypertrophy (LVH) and the expression of tumor necrosis factor-α (TNF-α) in the left ventricle of spontaneously hypertensive rats and the action mechanism were investigated. Normal Wistar-kyoto (WKY) rats were used as negative control, and spontaneously hypertensive rats (SHR) were randomly assigned to receive pla- cebo or SMB. SMB (1 g/kg·d) was injected intraperitoneally for 12 weeks. Systolic blood pressure (SBP) and left ventricular mass index (LVMI) were measured. HE, VG and immunohistochemical staining combined with computed morphometry were employed to evaluate the cardiomyocyte size, diameter, the collagen volume fraction (CVF), perivascular circumferential area (PVCA), and tumor necrosis factor-α (TNF-α) expression in the left ventricular tissue. The results showed, as compared with WKY rats, the SBP, LVMI, cardiomyocyte size, diameter, CVF, PCVA, and TNF-α expression were increased markedly in the 20-week-old spontaneously hypertensive rats. SMB decreased LVMI (P<0.01), size of cardiomyocytes (P<0.01), collagen volume fraction (P<0.01), perivascular circum- ferential area (P<0.01), and TNF-α expression (P<0.01), but had no effect on SBP (P>0.05). It was suggested that chronic administration of SMB could inhibit and reverse the development of LVH in spontaneously hypertensive rats independent of BP. TNF-α may be involved in the reversal mecha- nism of LVH by SMB.     

Study on effect and mechanism of essential garlic oil in inhibiting monocyte-vascular endothelial cell adhesion induced by interleukin-1α

Study on Effect and Mechanism of Essential Garlic Oil in Inhibiting MonocyteVascular Endothelial Cell Adhesion Induced by Interleukin-1α@葛璐璐@张薇@戴云@臧燕@黄纯洁     

Effects of activated protein C on coagulation and fibrinolysis in rabbits with endotoxin induced acute lung injury

Background Sepsis induced acute lung injury （ALI） as a common syndrome in clinical practice has a high mortality. Recombinant human activated protein C （APC） can significantly reduce the mortality of patients with severe sepsis. Several studies have implicated that APC may be protective in ALI. Methods Twenty-one rabbits were operatively prepared and randomly divided into sham, control, or APC groups （n=7 in each group）. After a tracheotomy had been performed, ALI was produced in the control and APC groups by infusion of Escherichia coil endotoxin 100 μg/kg per hour intravenously for 1 hour. The sham group received only the vehicle, infusion of 20 ml of 0.9% saline. The rabbits were studied under anesthesia for 6 hours and were ventilated with 40% oxygen. Bovine APC （25 μg·kg^-1·h^-1） was intravenously administered. The infusion was initiated half an hour post-injury and lasted for 4 hours. The animals were resuscitated with Ringer＇s lactate solution. Results In comparison with nontreatment in the control group, the infusion of APC significantly reduced the increase of thrombomodulin level （TM; control group was （0.68±0.06） ng/ml, vs APC group of （0.62±0.07） ng/ml at 6 hours, P 〈0.05）, and significantly attenuated the fall in protein S （PS; control group was （2.32±0.03） μg/ml at 2 hours, （2.24±0.06） μg/ml at 4 hours and （2.21±0.09）μg/ml at 6 hours, vs APC group （2.46±0.04） μg/ml at 2 hours, （2.40±0.05） μg/ml at 4 hours and （2.39±0.07） μg/ml at 6 hours, P 〈0.01）. In addition, APC limited the increase in plasminogen activator inhibitor-1 （PAI-1） both in plasma （control group was （0.68±0.12） ng/ml at 1 hour, （0.84±0.06） ng/ml at 2 hours, （0.87±0.08） ng/ml at 4 hours and （0.91±0.05） ng/ml at 6 hours, vs APC group （0.42±0.16） ng/ml at 1 hour, （0.43±0.04） ng/ml at 2 hours, （0.45±0.09） ng/ml at 4 hours and （0.45±0.14） ng/ml at 6 hours, P 〈0.01） and in bronchoalveolar lavage fluid （at 6 hour     

Molecular mechanism of endothelial cells about adhesion and proliferation in tissue engineering heart valve of seeding human umbilical vein endothelial cells on decellular porcine aortic valve

Objective To create the tissue engineering heart valve （TEHV） by seeding human umbilical vein endothelial cells （HUVECs） on decellular porcine aortic valve and investgate its mechanism of endothelial cells in adhesion and proliferation.Methods The porcine aortic valve was acellularized by using trypsin、EDTA、Triton X-100、RNase and DNase treatment.Biomechanical characteristics of fresh valves and acellularized valves were tested.     

Effect of Xuezhikang Capsule(血脂康胶囊)on Serum Tumor Necrosis Factor-αand Interleukin-6 in Patients with Nonalcoholic Fatty Liver Disease and Hyperlipidemia

<正>Objective:To evaluate the effect of Xuezhikang Capsule(血脂康胶囊) on the serum levels of inflammatory factors such as tumor necrosis factor-α(TNF-α) and interleukin-6(IL-6) in patients with nonalcoholic fatty liver disease(NAFLD) and hyperlipidemia,and to explore whether it has anti-inflammatory effect.Methods:A total of 84 patients were randomly assigned to two groups with stratified block randomization, the treatment group(42 cases) and the control group(42 cases).They were treated with Xuezhikang Capsule and polyene phosphatidylcholine capsule for twenty-four weeks,respectively.The changes in serum TNF-αand IL-6 were measured by enzyme linked immunosorbent assay before treatment and at the 12th and 24th week. Results:Compared with those before treatment,the serum levels of TNF-αand IL-6 significantly decreased in both groups after treatment(P0.01).There was no significant change between the two groups for the treatments at different time points(P0.05) and between the two groups for treatments at the same time points (P0.05).Conclusion:Xuezhikang Capsule can inhibit the serum inflammatory factor in patients with NAFLD and hyperlipidemia.     

Advanced glycation end products inhibit production and activity of matrix metalloproteinase-2 in human umbilical vein endothelial cells

Objective It has been reported that advanced glycation end products (AGEs) participate in pathogenesis of accelerated atherosclerosis in diabetes through damaging endothelial function. Matrix metalloproteinases (MMPs) can be synthesized by endothelial cell and contribute to maintain endothelial homeostasis. The present work are aimed at     

Effect of Tumor Necrosis Factor-α Antagonism in Asthma： a Meta-analysis of the Published Literature

It remains controversial whether tumor necrosis factor(TNF)-α antagonism is effective for asthma.This meta-analysis was performed to evaluate efficacy of TNF-α antagonism in treatment of patients with asthma.MEDLINE,EMBASE,LILACS,and CINAHL databases were searched for English-language studies published through January 3,2010.Randomized-controlled trials comparing TNF-α antagonism with control therapy were selected.For each report,data were extracted in relation to the outcomes analyzed:asthma exacerbation,asthma quality of life questionnaire scores,and forced expiratory volume in 1 second.Four assessable trials were identified including 641 patients with asthma.TNF-α antagonism therapy was superior to control therapy in preventing exacerbations in asthmatics [pooled odds ratio 0.52(95% confidence interval 0.29-0.88),P=0.02];however,there was a nonsignificant reduction in asthma quality of life questionnaire scores [0.23(0 to 0.47),P=0.05],forced expiratory volume in 1 second [0.03,(-0.14 to 0.10),P=0.74] when analyzed using standardized mean differences.TNF-α antagonism was superior to control chemotherapy in terms of asthma exacerbation,but not asthma quality of life questionnaire scores or forced expiratory volume in 1 second.     

Pharmacodynamic study of recombinant human erythropoietin on a renal anemia model induced by gentamycin in rats

ＰｈａｒｍａｃｏｄｙｎａｍｉｃｓｔｕｄｙｏｆｒｅｃｏｍｂｉｎａｎｔｈｕｍａｎｅｒｙｔｈｒｏｐｏｉｅｔｉｎｏｎａｒｅｎａｌａｎｅｍｉａｍｏｄｅｌｉｎｄｕｃｅｄｂｙｇｅｎｔａｍｙｃｉｎｉｎｒａｔｓＣａｏＺｈｉｆａｎｇ（曹之舫）；ＪｉａＬｉｎ（贾林）；Ｊｉ...     

Effect of Tumor Necrosis Factor-α on Acyl Coenzyme A： Cholesteryl Acyltransferase Activity and ACAT1 Gene Expression in THP-1 Macrophages

In order to explore the effect and mechanisms of tumor necrosis factor-α (TNF-α) on the activity of the acyl coenzyme A: cholesteryl acyltransferase (ACAT), THP-1 monocytes were cul- tured and induced to differentiate into macrophages with phorbol ester. TNF-α (60 ng/mL) was added at different time points into the macrophage-containing medium and the ACAT enzyme activity was measured by quantifying the incorporation of 1-14C oleoyl CoA into cholesteryl esters. The expres- sion of ACAT-1 protein and mRNA was respectively detected by Western blotting and RT-PCR in THP-1 macrophages 24 h after treatment with TNF-α (60 ng/mL). The results indicated that ACAT activity in THP-1 macrophages treated with TNF-α was increased in a time-dependent manner. The expression levels of ACAT-1 protein and mRNA were significantly increased in THP-1 macrophages after treatment with TNF-α (P<0.05). It was suggested that TNF-α could increase the activity of ACAT in THP-1 macrophages by up-regulating the expression of ACAT-1 gene.     

Effect of Mifepristone on Transforming Growth Factor-β and its Receptor Transcription in Decidua, Villi and Serum Tumor Necrosis Factor -α Level in Early Human Gestation

Mifepristone is a progesterone antagonist which acts at the level of the receptor. Itbinds the progesterone receptor with a high affinity and antagonises progesterone biologicalaction. It has been applied in clinical use for multiple therapeutic purposes. In obstetrics andgynecology, mifepristone has been effective in medical termination of pregnancy in the firsttrimester. Mifepristone followed approximately 48 h later by a prostaglandin analog hasbeen reported to effect complete abortion in 9…     

Effect of serum from overfatigue rats on JNK/c-Jun/HO-1 pathway in human umbilical vein endothelial cells and the intervening effect of Tongxinluo (通心络) superfine powder

Objective:To cultivate human umbilical vein endothelial cells (HUVECs) in the serum of overfatigue rats with the intervention of Tongxinluo (通心络) superfine powder (TXLSP).By examining the variation of the activity of JNK/c-Jun/HO-1 pathway,the possible mechanisms of vascular endothelial dysfunction under overfatigue conditions and the intervening effect of TXLSP were explored.Methods:The HUVECs were randomly divided into the normal control group,the model group,the SP600125 (a specific antagonist of JNK)...     

Cardiotrophin-1 induces intercellular adhesion molecule-1 expression by nuclear factor κB activation in human umbilical vein endothelial cells

Background In addition to elevated concentrations of cytokines, patients with congestive endothelial dysfunction and increased plasma concentrations of adhesion molecules heart failure （CHF） show ke intercellular adhesion molecule-1 （ICAM-1）. Furthermore, the concentration of cardiotrophin-1 （CT-1） - a cytokine of the interleukin-6 superfamily - is increased in CHF. We tested the hypothesis whether CT-1 is able to induce ICAM-1 in human umbilical vein endothelial cells （HUVEC）. Furthermore we examined the signalling mechanisms of CT-1 mediated ICAM-1 expression. Methods Confluent layers of HUVEC were incubated with increasing concentrations of CT-1 （5 to 100 ng/ml） for different periods. ICAM-1 mRNA was determined by real-time polymerase chain reaction （PCR） and ICAM-1 surface expression by fluorescence-activated cell sorter （FACS） analysis and soluble ICAM-1 （slCAM-1） in the culture supernatant by enzyme linked immunosorbent assay （ELISA）. To clarify the signalling pathway of CT-1 induced ICAM-1 expression we used various inhibitors of possible signal transducing molecules, electromobility shift assay （EMSA） and Western blot analysis. Results CT-1 induced ICAM-1 mRNA （1.8±0.8 fold increase compared to unstimulated cells after 6 hours） and protein （1.4±0.2 fold increase compared to unstimulated cells after 48 hours） in HUVEC in a time- and concentration-dependent manner. EMSA experiments show that CT-1 causes nuclear factor （NF） κB activation. Because parthenolide could inhibit CT-1 induced ICAM-1 expression NFκB activation is required in this pathway. CT-1 did not activate extracellular signal regulated kinases （ERK）, c-Jun N-terminal kinase （JNK） and p38. Conclusion CT-1 is able to induce ICAM-1 in endothelial cells by NFκB activation. These results may explain in part elevated ICAM-1 concentrations in patients with CHF and endothelial dysfunction.     

Dynamic Expression of Tumor Necrosis Factor-α and Vascular Endothelial Growth Factor in Rat Model of Pulmonary Emphysema Induced by Smoke Exposure

In order to explore the roles of tumor necrosis factor-α(TNF-α) and vascular endothelial growth factor(VEGF) in the pathogenesis of pulmonary emphysema,male Wistar rats were randomized into group A1,group A2.5 and group A4,each with smoke exposure for 1 month,2.5 months or 4 months,respectively.Group B1,group B2.5 and group B4 were used as non smoking controls at corresponding time points.TNF-α in bronchoalveolar lavage fluid(BALF) and expression of VEGF in lung tissue was determined by ELISA or by SABC immunohistochemistry assay either.Lung slices were stained with hematoxylin and eosin(HE).Results showed that in animal with smoke exposure the mean linear interceptor(Lm),an index of pulmonary emphysema and the content of TNF-α in BALF increased gradually,on contrary,the expression of VEGF in lung tissue decreased(P<0.05).This phenomenon was not obvious in animals without smoke exposure.Lm was negatively correlated to the VEGF expression(γ=-0.81,P<0.01) and positively correlated to TNF-α concentration(γ = 0.52,P<0.004),which implies that smoke exposure decreased the expression of VEGF and increased the expression of TNF-α.It is plausible to speculate that the imbalance of TNF-α and VEGF may play an important role in the pathogenesis of smoke-induced pulmonary emphysema.