Search results for: Myeloperoxidase Inhibitor
#29339045 // Save this To Up
Deficiency of dietary pyridoxine disturbed the intestinal physical barrier function of young grass carp (Ctenopharyngodon idella).The aim of this study was to assess the effects of dietary pyridoxine (PN) deficiency on intestinal antioxidant capacity, cell apoptosis and intercellular tight junction in young grass carp (Ctenopharyngodon idella). A total of 540 young grass carp (231.85 ± 0.63 g) were fed six diets containing graded levels of PN (0.12-7.48 mg/kg diet) for 10 weeks. At the end of the feeding trial, the fish were challenged with Aeromonas hydrophila for 2 weeks. The results showed that compared with the optimal PN level, PN deficiency (1) increased the contents of reactive oxygen species (ROS), malondialdehyde (MDA) and protein carbonyl (PC), decreased the activities and mRNA levels of antioxidant enzymes such as copper, zinc superoxide dismutase (CuZnSOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST) and glutathione reductase (GR) (P < .05); (2) up-regulated the mRNA levels of cysteinyl aspartic acid-protease-3 (caspase-3), caspase-7, caspase-8, caspase-9, Bcl-2 associated X protein (Bax), apoptotic protease activating factor-1 (Apaf-1) and Fas ligand (FasL), and down-regulated the mRNA levels of inhibitor of apoptosis proteins (IAP), B-cell lymphoma protein-2 (Bcl-2) and myeloid cell leukaemia-1 (Mcl-1) (P < .05); (3) down-regulated the mRNA levels of ZO-1, occludin [only in middle intestine (MI)], claudin-b, claudin-c, claudin-f, claudin-3c, claudin-7a, claudin-7b and claudin-11, and up-regulated the mRNA levels of claudin-12 and claudin-15a (P < .05), which might be partly linked to Kelch-like-ECH-associated protein 1a (Keap1a)/NF-E2-related factor 2 (Nrf2), p38 mitogen-activated protein kinase (p38MAPK) and myosin light chain kinase (MLCK) signalling in the intestines of fish. However, the activities and mRNA levels of MnSOD, the mRNA levels of Keap1b, c-Jun N-terminal protein kinase (JNK) and claudin-15b in three intestinal segments, and the mRNA levels of occludin in the proximal intestine (PI) and distal intestine (DI) were not affected by graded levels of PN. These data indicate that PN deficiency could disturb the intestinal physical barrier function of fish. Additionally, based on the quadratic regression analysis for MDA content and GST activity, the dietary PN requirements for young grass carp were estimated as 4.85 and 5.02 mg/kg diet, respectively.
2024 related Products with: Deficiency of dietary pyridoxine disturbed the intestinal physical barrier function of young grass carp (Ctenopharyngodon idella).Ofloxacin CAS Number [824 BACTERIOLOGY BACTEROIDES TCP-1 theta antibody Sour Recombinant Thermostable Recombinant Thermostable Recombinant Thermostable Recombinant Carp GH Prote Recombinant Carp GH Prote Recombinant Carp GH Prote Recombinant Human PKC the Recombinant Human PKC the Recombinant Human PKC the
#29333048 // Save this To Up
Astaxanthin Ameliorates Hepatic Damage and Oxidative Stress in Carbon Tetrachloride-administered Rats.Astaxanthin is of carotenoids group which possess strong antioxidant properties. The present study was conducted to evaluate the hepatoprotective effects of astaxanthin in carbon tetrachloride (CCl4)-treated rats.
2408 related Products with: Astaxanthin Ameliorates Hepatic Damage and Oxidative Stress in Carbon Tetrachloride-administered Rats.OXI TEK (Oxidative Stress Anti beta3 AR Human, Poly 8 Isoprostane oxidative s Transcription factors: O 3 Cyanoindole (Indole 3 c OxiSelect™ Cellular UV- Interleukin-34 IL34 (N-t Interleukin-34 IL34 anti Sterile filtered goat se Sterile filtered goat se Sterile filtered mouse s Sterile filtered rat ser
#29331766 // Save this To Up
Roflumilast, type 4 phosphodiesterase inhibitor, attenuates inflammation in rats with ulcerative colitis via down-regulation of iNOS and elevation of cAMP.Roflumilast (Rof), a phosphodiesterase 4 (PDE4) inhibitor, has been shown to be an effective agent in inflammatory diseases and marketed for chronic obstructive pulmonary disease.
2375 related Products with: Roflumilast, type 4 phosphodiesterase inhibitor, attenuates inflammation in rats with ulcerative colitis via down-regulation of iNOS and elevation of cAMP.ZSTK-474 Mechanisms: PI3K MEK-162 (ARRY-438162) Mec MLN-4924 Mechanisms: NAE TAK-441 Mechanisms: Hedge AZD-4547 Mechanisms: FGFR Inflammation (Human) Anti Inflammation (Mouse) Anti Inflammation (Human) Anti Inflammation (Mouse) Anti Inflammation (Human) Quan Inflammation (Mouse) Quan Rabbit Anti-NOS-2 iNOS Po
#29324628 // Save this To Up
Ulinastatin Protects Against LPS-Induced Acute Lung Injury by Attenuating TLR4/NF-κB Pathway Activation and Reducing Inflammatory Mediators.Acute lung injury (ALI) and its severe form, acute respiratory distress syndrome (ARDS), remain the leading causes of morbidity and mortality in intensive care units. Ulinastatin (UTI), a serine protease inhibitor, possesses anti-inflammatory properties and has been suggested to modulate lipopolysaccharide (LPS)-induced sepsis; thus, it is now widely used in the treatment of pancreatitis, sepsis, and septic shock. Toll-like receptor 4 (TLR4), an essential LPS signaling receptor, plays a critical role in the activation of innate immunity. The aim of this study was to investigate whether UTI alleviates ALI by attenuating TLR4 expression and to explore the underlying molecular mechanisms involved. Male C56BL/6 mice were administered UTI intravenously 1 h before and 6 h after exposure to LPS by intra-tracheal instillation. Human lung epithelial (BEAS-2B) cells were incubated with LPS in the presence or absence of UTI. An enzyme-linked immunosorbent assay was used to detect levels of inflammatory cytokines. Western blot analysis was performed to detect changes in TLR4 expression and nuclear factor-κB (NF-κB) activation. UTI significantly protected animals from LPS-induced ALI, decreasing the lung wet/dry weight ratio, ALI score, total cells, neutrophils, macrophages, myeloperoxidase activity, and malondialdehyde content, factors associated with lung histological damage. UTI treatment also markedly attenuated levels of TLR4 and other pro-inflammatory cytokines. Furthermore, UTI significantly attenuated LPS-induced increases in TLR4 protein expression and NF-κB activation in lung tissues. Similarly, UTI markedly attenuated TLR4 expression and NF-κB activation in LPS-stimulated BEAS-2B cells. These findings indicate that UTI ameliorates LPS-induced ALI by attenuating the TLR4/NF-κB pathway activation.
2068 related Products with: Ulinastatin Protects Against LPS-Induced Acute Lung Injury by Attenuating TLR4/NF-κB Pathway Activation and Reducing Inflammatory Mediators.NF-kB Phospho-Specific Ar NF-kB II Phospho-Specific Anti-AICDA(Activation-ind Anti AICDA(Activation ind TLR4 Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Human Macrophage Inflamma Human Macrophage Inflamma Human Macrophage Inflamma
#29323739 // Save this To Up
Fasudil alleviates pressure overload-induced heart failure by activating Nrf2-mediated antioxidant responses.The RhoA/Rho-kinase cascade plays an important role in many aspects of cardiovascular function. This study aims to investigate the protective effects of fasudil, a Rho-kinase inhibitor, on pressure overload induced heart failure in rats. Pressure overload induced heart failure was induced in SD rats by banding the abdominal aorta for 8 weeks. The rats were divided into four groups: Sham, TAC, TAC plus low dose of fasudil and TAC plus high dose of fasudil group. Low dose and high dose fasudil were 5 mg/kg/day and 10 mg/kg/day respectively. Rats in the Sham and TAC groups were treated with vehicle. Fasudil effectively inhibited TAC-induced heart failure, as evaluated by echocardiography and transmission electron microscopy. Fasudil could significantly promote superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activity and significantly decrease malondialdehyde (MDA) content in a dose-dependent maner in TAC rats. Consistently, fasudil evoked significant nuclear translocation of Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) with increased DNA/promoter binding and transactivation of Nrf2 targets. In addition, fasudil increased the content of iron as well as transferrin receptor1 (TfR1) in TAC rats. A mild oxidative stress induced by iron may activate the antioxidant enzymes by feedback response. Taken together, these results indicate that the protective effect of fasudil may be due to its strong antioxidative activities which related with the activated Nrf2 and its down-regulated genes. These findings provide a new treatment concept and support the benefit of fasudil treatment in heart failure. This article is protected by copyright. All rights reserved.
2727 related Products with: Fasudil alleviates pressure overload-induced heart failure by activating Nrf2-mediated antioxidant responses.Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Human Epstein-Barr Virus Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Mouse Anti-Human Fas CD95 Mouse Anti-Human Fas CD95 Fasudil, Monohydrochlorid
#29318737 // Save this To Up
Involvement of p38MAPK in Impaired Neutrophil Bactericidal Activity of Hemodialysis Patients.Mortality from infections has been reported to be higher in hemodialysis (HD) patients. Although dysfunction of neutrophils against bacterial infection was reported in HD patients, the precise mechanism remains to be clarified. We therefore examined the impacts of neutrophil inflammatory signaling on bactericidal activity in HD patients. Comprehensive analyses of intracellular signalings were performed in whole blood of HD patients and control using a microarray system. To confirm the contribution of the signaling to bactericidal activity in neutrophils, we examined the phosphorylation, bacterial killing function, reactive oxygen species (ROS) production, and myeloperoxidase (MPO) release in neutrophils against Staphylococcus aureus. RNA microarray analysis showed the suppression of p38 mitogen activated protein kinase (MAPK) signaling in HD patients. Neutrophils in HD patients showed the impairment of bactericidal activity against S. aureus compared to healthy subjects. Phosphorylation rate of p38MAPK of neutrophils in response to S. aureus was lower in HD patients than healthy subjects. The levels of ROS produced by neutrophils after co-culture with S. aureus were lower in HD patients, on the other hand, there was no difference of MPO release between HD patients and healthy subjects. A selective pharmacological inhibitor of p38MAPK suppressed bacterial killing function as well as ROS production in neutrophils of healthy subjects. Impairment of p38MAPK signaling pathway might contribute to the suppression of neutrophil bactericidal activity in HD patients through less production of ROS.
2272 related Products with: Involvement of p38MAPK in Impaired Neutrophil Bactericidal Activity of Hemodialysis Patients.Cell Meter™ Fluorimetri Cell Meter™ Fluorimetri Alkaline Phospatase (ALP) ELISA kit CLGI,Collagenas EnzyChrom™ Kinase Assay Mouse Anti-Lipoprotein Li Neutrophil Elastase Inhib MarkerGeneTM in vivo lacZ MarkerGeneTM Live Dead As Resorufin Oleate, Fluorog Ofloxacin CAS Number [824 EpiQuik Histone Methyltra
#29306874 // Save this To Up
A Structurally Dynamic N-terminal Region Drives Function of the Staphylococcal Peroxidase Inhibitor (SPIN).The heme-containing enzyme myeloperoxidase (MPO) is critical for optimal antimicrobial activity of human neutrophils. We recently discovered that the bacterium Staphylococcus aureus expresses a novel immune evasion protein, called SPIN, that binds tightly to MPO, inhibits MPO activity, and contributes to bacterial survival following phagocytosis. A co-crystal structure of SPIN bound to MPO suggested that SPIN blocks substrate access to the catalytic heme by inserting an N-terminal β-hairpin into the MPO active site channel. Here, we describe a series of experiments that more completely define the structure/function relationships of SPIN. Whereas the SPIN N-terminus adopts a β-hairpin confirmation upon binding to MPO, solution NMR studies presented here are consistent with this region of SPIN being dynamically structured in the unbound state. Curiously, while the N-terminal β-hairpin of SPIN accounts for ~55% of the buried surface area in the SPIN/MPO complex, its deletion did not significantly change the affinity of SPIN for MPO but did eliminate the ability of SPIN to inhibit MPO. The flexible nature of the SPIN N-terminus rendered it susceptible to proteolytic degradation by a series of chymotrypsin-like proteases found within neutrophil granules, thereby abrogating SPIN activity. Degradation of SPIN was prevented by the S. aureus immune evasion protein Eap, which acts as a selective inhibitor of neutrophil serine proteases. Together, these studies provide insight into MPO inhibition by SPIN and suggest possible functional synergy between two distinct classes of S. aureus immune evasion proteins.
2519 related Products with: A Structurally Dynamic N-terminal Region Drives Function of the Staphylococcal Peroxidase Inhibitor (SPIN).Goat Anti-Human Glutathio Goat Anti-Human Glutathio Anti-human C1 Esterase In Anti human C1 Esterase In Anti-Axin1 (C-terminal re Anti Axin1 (C terminal re HIV 1 gag p24 recombinant HIV 1 nef recombinant ant HIV 1 env gp41 recombinan HIV 2 env gp36 recombinan HCV NS3 1359 1456aa antig HIV 1 intergase antigen.
#29301535 // Save this To Up
Inhibition of histone-deacetylase activity rescues inflammatory cystic fibrosis lung disease by modulating innate and adaptive immune responses.Chronic lung disease resulting from dysfunctional cystic fibrosis transmembrane conductance regulator (CFTR) and NFκB-mediated neutrophilic-inflammation forms the basis of CF-related mortality. Here we aimed to evaluate if HDAC inhibition controls Pseudomonas-aeruginosa-lipopolysaccharide (Pa-LPS) induced airway inflammation and CF-lung disease.
1473 related Products with: Inhibition of histone-deacetylase activity rescues inflammatory cystic fibrosis lung disease by modulating innate and adaptive immune responses.EpiQuik Histone Methyltra EpiQuik Histone Methyltra EpiQuik Histone Methyltra EpiQuik Histone Methyltra EpiQuik Histone Methyltra EpiQuik Histone Methyltra Lung disease spectrum tis Mouse Anti-Lipoprotein Li Lung disease spectrum tis Lung disease spectrum (pu Lung disease spectrum tis Lung disease spectrum (pu
#29289364 // Save this To Up
Imatinib Is Protective Against Ischemia-Reperfusion Injury in an Ex Vivo Rabbit Model of Lung Injury.Ischemia-reperfusion injury is characterized by an increase in oxidative stress and leads to significant morbidity and death. The tyrosine kinase c-Abl is activated by oxidative stress and mediates processes that affect endothelial barrier function. We hypothesized treatment with the c-Abl inhibitor imatinib would be protective against ischemia-reperfusion injury in our ex vivo rabbit model.
1734 related Products with: Imatinib Is Protective Against Ischemia-Reperfusion Injury in an Ex Vivo Rabbit Model of Lung Injury.Interleukin-34 IL34 (N-t Interleukin-34 IL34 anti interleukin 17 receptor C Rabbit Anti-NOS-2 iNOS Po Rabbit Anti-NOS-2 iNOS Po Rabbit Anti-NOS-2 iNOS Po Rabbit Anti-NOS-2 iNOS Po Rabbit Anti-NOS-2 iNOS Po Rabbit Anti-NOS-2 iNOS Po Rabbit Anti-NOS-2 iNOS Po Rabbit Anti-Insulin Recep Rabbit Anti-Insulin Recep
#29284473 // Save this To Up
Involvements of p38 MAPK and oxidative stress in the ozone-induced enhancement of AHR and pulmonary inflammation in an allergic asthma model.Exposure to ambient ozone (O3) increases the susceptivity to allergens and triggers exacerbations in patients with asthma. However, the detailed mechanisms of action for O3 to trigger asthma exacerbations are still unclear.
2777 related Products with: Involvements of p38 MAPK and oxidative stress in the ozone-induced enhancement of AHR and pulmonary inflammation in an allergic asthma model.Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon TGF beta induced factor 2 Anti beta3 AR Human, Poly GPCR Signaling to MAPK ER MAPK Phospho-Specific Arr Inflammation (Human) Anti Inflammation (Mouse) Anti Inflammation (Human) Anti Inflammation (Human) Anti
Voortstraat 49, 1910 Kampenhout BELGIUM
Tel 0032 16 58 90 45 Fax 0032 16 50 90 45
9, rue Lagrange, 75005 Paris
Tel 01 43 25 01 50 Fax 01 43 25 01 60
52062 Aachen Deutschland
Tel 0241 40 08 90 86 Fax 0241 55 91 05 36
Howard Frank Turnberry House
1404-1410 High Road
Whetstone London N20 9BH
Tel 020 3393 8531 Fax 020 8445 9411
Schweiz Züri +41435006251
Česká republika Praha +420246019719
Ireland Dublin +35316526556
Norge Oslo +4721031366
Finland Helsset +358942419041
Sverige Stockholm +46852503438
Ελλάς Αθήνα +302111768494
Magyarország Budapest +3619980547
GENTAUR Poland Sp. z o.o.
ul. Grunwaldzka 88/A m.2
81-771 Sopot, Poland
Tel 058 710 33 44
Fax 058 710 33 48
GENTAUR Nederland BV
5521 DG Eersel Nederland
Tel 0208-080893 Fax 0497-517897
Piazza Giacomo Matteotti, 6, 24122 Bergamo
Tel 02 36 00 65 93 Fax 02 36 00 65 94
53 Iskar Str. 1191 Kokalyane, Sofia