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Garlichasbeenusedasaneffectivemedicineforcenturies.Inrecentyears,garlichasattractedmoreattentionduetoitsprotec tiveeffectsagainstcardiovasculardiseases.Vascularcelladhesivemolecule 1 (VCAM 1,CD1 0 6)isamemberofimmunoglobulinsuperfamily.Theadhesivemolecule…  相似文献   

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Endometriosisisamongthemostcom-mongynecologicentities,characterizedbyectopicgrowthofendothelialtissueintheperitonealcavity.Althoughthepathogene-sisisstillpoorlyunderstood,aconsistentfindingintheperitonealfluidofthesepa-tientshasbeentheincreasednumber…  相似文献   

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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.  相似文献   

6.
The focal influx and accumulation of lipoprotein at arterial lesion--prone sites and the recruitment of blood monocytes to those sites are two early key events in atherogenesis. After entering thesubendothelial space of the arterial wall, monocytes undergo activation--differentiation to becomemacrophages which subsequently internallze oxidatively modified lipoproteins through scavenger receptors and become foam cells. Therefore, tostudy the mechanism of the recruitment of bloodmonocytes to the…  相似文献   

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The hypoxic model to simulate hypoxic microenvironment in solid tumors was established and the effect of hydrocamptothecin (HCPT) on the hypoxia-induced over-expression of HIF-1α and VEGF genes was explored. Human cervical cancer SiHa cells were cultured in vitro under hypoxic conditions (37℃, 5% CO2, 1%O2) and treated with different concentrations of HCPT for 24 h. The mRNA and protein expression levels of HIF-1α, VEGF and Glutl in SiHa cells were detected by semi-quantitative RT-PCR and Western blot respectively. Normoxic control groups were exposed to normoxic conditions for 24 h. Under normoxic conditions, HCPT had no obvious effects on the HIF-1α and VEGF gene expression. Hypoxia induced the up-regulation of HIF-1α protein and downstream VEGF gene, and HCPT showed a dose-dependently inhibitory effect on the hypoxia-induced over-expression of HIF-1α protein and VEGF gene expression in SiHa cells, whereas HCPT had no significant effect on the HIF-1α mRNA expression. No difference in HCPT cytotoxic- ity was observed between hypoxic groups and normoxic control groups. It was suggested that HCPT could inhibite the expression of HIF-1α protein and downstream VEGF gene in hypoxic SiHa cells in a dose-dependent manner, and the inhibitory effect was not related with HCPT cytotoxicity.  相似文献   

8.
In order to investigate the role of TNF-α and ICAM-1 in the pathogenesis of lichen planus, immunohistochemistry was used to detect the expression of TNF-α and ICAM-1 in skin le- sions of the patients with lichen planus and skin tissues of normal subjects. The results showed that positive rates of TNF-α and ICAM-1 expressions in lichen planus were significantly higher than those in normal skins (both P<0.05). Meanwhile, there was a obvious correlation between the in- crease of TNF-α and that of ICAM-1 in lichen planus. The expression of TNF-α and ICAM-1 might play an important role in the development of lichen planus.  相似文献   

9.
Autoi mmune myocarditis in Coxsackievirus B3(CB3)-infected mice is associated with infiltrationof the heart by inflammatory cells that secreteTNF-αand IL-1[1].In this study we examine theexpression of cytokines , TNF-αand IL-1βpro-duced locallyinthe heart inresponse to MCMVin-fectionin order to determine their potential role inthe development of acute myocarditis .1MATERIALS AND METHODS1 .1Reagents and AntibodiesMonoclonal goat anti-mouse IL-1β, TNF-αanti-body and SABC …  相似文献   

10.
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.  相似文献   

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To investigate the effect of the Ginkgo Biloba Extract (GBE) on the asthma and examine its possible mechanisms, 75 asthma patients were divided into 4 groups and the patients were respectively treated with fluticasone propionate for 2 weeks or 4 weeks, or treated with fluticasone propionate plus GBE for 2 weeks or 4 weeks. Fifteen healthy volunteers served as healthy controls. Sputum inhalation with inhaling hypertonic saline (4%-5%) was performed. Lung ventilatory function and forced expiratory volume in one second (FEVI) were measured. The numbers of different cells in induced sputum were calculated. The expression of PKCα in the cells was immunocytochemically detected and the percentages of positive cells in different cells were counted. Interleukin-5 (IL-5) in sputum supernatants was detected with enzyme-linked immunosorbent assay. The percentage of eosinophils, lymphocytes, PKCα positive inflammatory cells and the concentration of IL-5 in asthmatic patients were higher than those in the controls (P〈0.05), and the eosinophils, lymphocytes, positive expression of PKCα and the level of IL-5 were significantly decreased in asthmatic patients after they were treated with fluticasone propionate or fluticasone propionate plus GBE. However, they were still significantly higher than those of the controls. Compared to the group treated with glucocorticosteroid for 2 weeks, no significant decrease was found in the percentage of eosinophils, lymphocytes, PKCα positive inflammatory cells and the IL-5 in the supernatant of induced sputum. Compared with the group treated with glucocorticosteroid for 2 or 4 weeks, significant decrease in the same parameters was observed in the group treated with fluticasone propionate and GBE for 4 weeks. The IL-5 level in the supernatant of induced sputum was positively correlated with the percentage of PKCα-positive inflammatory cells and the percentage of eosinophils in the induced sputum in asthma patient groups respectively (n=150, r=0.83, P〈0.01; n=150,  相似文献   

12.
p38 mitogen-activated protein kinase (p38MAPK) is a member of the mitogen-activated protein kinase (MAPK) family, p38MAPK pathway is one of the most widely studied signaling pathways involved in the transduction of intracellular signals including survival, growth, differentiation and death. Monocyte chemoattractant pro-  相似文献   

13.
L- Tetrahydropalmatine (L- THP) ,a kind of al-kaloid extracted from traditional Chinese medicineRhizoma corydalis,posseses sedative,analgesic andhypnotic effects.Recently,it has been demonstratedthat L- THPalso had calcium- antagonistic and antiar-rythmic effects.Studies showed that L- THP had aprotective effect on acute focal and global cerebral is-chemia- reperfusion injury[1,2 ] .Many studies provedthat the production of NO wasincreased significantlyduring ischemia- reperfusion.The o…  相似文献   

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Objective: To explore the effects of Houttuynia Cordata Thumb (HCT 鱼腥草 Yu Xing Cao) on expression of transforming growth factor-β1 (TGF-β1) and bone morphogenetic protein-7 (BMP-7) in the renal tissues of diabetic rats. Methods: The diabetic rats induced by intravenous injection of streptozotocin(STZ) were randomly divided into a model group, a HCT group and a lotensin group, with normal rats designated as the controls. 8 weeks later, the ratio of kidney weight to body weight, the glomerular area, the excretion of β 2-microglobin (β2-MG) in 24-hr urine, the albumin excretion in 24-hr urine, and creatinine clearance rate (CCR) were investigated. The expression of TGF- β 1, BMP-7 and collagen I in the renal tissues was observed with the immunohistochemical method and by the semi-quantitative assay. Results: The overgrowth of glomerulus, the excretion of β 2-MG in 24-hr urine, the albumin excretion rate in 24-hr urine and CCR in the HCT group significantly reduced (P〈0.05), and the expression of TGF-β1 and collagen I significantly decreased (P〈0.05), but BMP-7 significantly increased (P〈0.05) in the HCT group as compared with those in the model group, with no significant difference as compared with the lotensin group (P〉0.05). Conclusion: HCT has a protective effect on the renal tissues in diabetic rats, which is probably correlated with the decrease of the expression of TGF-β1 and collagen I and with the increase of the expression of BMP-7 in the renal tissues.  相似文献   

15.
Bronchialasthmaisadiseaseofchronicairwayinflammationwhichinvolvesavarietyofcellsin cludingmastocytes,granulocytes,lymphocytesetc,inwhichlymphocytesplayanespeciallyim portantpart,buttheexactmechanismshavenotbeenfullyunderstoodyet.ZayasuetalfoundthattheCOlevelsignificantlyincreasedinasthmapa tients'expiredgas,andthusinferredthatendoge neticCOmightbeinvolvedinthepathogenesisofasthma[1].EndogeneticCOoriginatesfromproto hemedegradationandintheprocesshemeoxygen ase(HO)actsasbothinitiationandrestr…  相似文献   

16.
Chemokinesaresecretedproinflammatorycytokinesthatattractandactivateinflammatorycellsandplayacriticalroleintheinitiationandmaintenanceofthein flammatoryresponse.Accumulatingevidencesuggeststhatsupramaximalconcentrationofcholecystokininin ducestheexpression…  相似文献   

17.
3, 4 dihydroxyacetophenone ( DHAP) is anactive component isolated from leaves of Tuma odongqing ( Ilex Pubescens Hook. Et Arn. Varglaber Chang), a Chinese traditional herb. It is in itially used to promote blood circulation and re move blood stasis[1, 2]. Previous experimental andclinical data proved that it could regulate the bal ance between TXA2 and PGI2, cause vesodilationand inhibit platelet aggregation[3]. It has showed agood curative effect in the…  相似文献   

18.
Bronchioalveolar carcinoma (BAC) was classified into lung adenocarcinoma in WHO types. Itwas reported that the increase in adenocarcinomawas due to an increase in BAC[1]. The histogenesisfor BAC was nuclear now. al--antitrypsinase (alAT) is an protease inhibitor mainly synthesizedand secreted by hepatocytes, which can inhibit theactivities of various protein hydrolases and limitthe growth and diffusion of tumor cells to some extent. Several studies demonstrated that al--ATcould be expres…  相似文献   

19.
To observe the alteration in the expression of DNA repair enzymes hOGG1 and hMYHa and the change in 8-OHdG levels in the HBx gene-transfected cells HepG2/HBx and to explore the mechanisms of the HBV-associated hepatocellular carcinoma, the gene-transfected cells HepG2/HBx which stably expressed HBx was established, and the effect of HBx on the cell cycle and proliferation of HepG2 was examined. By using the β-actin as the interior control, real-time polymerase chain reaction (Real-time qPCR) was employed to quantitatively detect the expression of DNA repair enzymes hOGG1 and hMYHα in the HepG2/HBx, the control cells HepG2 and HepG2 transfected with pcDNA3.1 vector (HepG2/pDNA3.1). The 8-OHdG levels were determined by HPLC/ECD in the established gene-transfected cells HepG2/HBx and the control cells HepG2 and HepG2/pcDNA3.1. Our results showed that the expression of DNA repair enzyme hMYHα in the HepG2/HBx (0.021±0.007) was significantly lower than that of HepG2 (0.099±0.041) (P〈0.05) and HepG2/pDNA3.1 (0.121±0.005) (P〈0.05). However, the no significant differences existed in the expression of DNA repair enzyme hOGG1 among the three cell strains (P〉0.05). The 8-OHdG level in the HepG2/HBx was significantly higher than that in HepG2 and HepG2/pcDNA3.1 (P〈0.05). It is concluded that HBx gene may inhibit the expression of DNA repair enzyme hMYHα mRNA to impair the ability to repair the intracellular DNA oxidative damage, to increase the oxidative DNA-adduct 8-OHdG and to affect the nucleotide excision repair function, thus participate in the occurrence and development of hepatocellular carcinoma.  相似文献   

20.
Objective PERK/eI F2α/CHOP is a major signaling pathway mediating endoplasmic reticulum(ER) stress related with atherosclerosis.Oxidized LDL(ox-LDL) also induces endothelial apoptosis and plays a vital role in the initiation and progression of atherosclerosis.The present study was conducted to explore the regulatory effect of ox-LDL on PERK/e IF2α/CHOP signaling pathway in vascular endothelial cells.Methods The effects of ox-LDL on PERK and p-e IF2α protein expression of primary human umbilical vein endothelial cells(HUVECs) were investigated by Western blot analysis.PERK gene silencing and selective eI F2α phosphatase inhibitor,salubrinal were used to inhibit the process of ox-LDL induced endothelial cell apoptosis,caspase-3 activity,and CHOP mR NA level.Results Ox-LDL treatment significantly increased the expression of PERK,PERK-mediated inactivation of e IF2α phosphorylation,and the expression of CHOP,as well as the caspase-3 activity and apoptosis.The effects of ox-LDL were markedly decreased by knocking down PERK with stable transduction of lentiviral sh RNA or by selective eI F2α phosphatase inhibitor,salubrinal.Conclusion This study provides the first evidence that ox-LDL induces apoptosis in vascular endothelial cells mediated largely via the PERK/eI F2α/CHOP ER-stress pathway.It adds new insights into the molecular mechanisms underlying the pathogenesis and progression of atherosclerosis.  相似文献   

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