Search results for: Anti Human Brain Derived Neurotrophic Factor (BDNF)
#31687714 // Save this To Up
Ingestion of Bifidobacterium longum subspecies infantis strain CCFM687 regulated emotional behavior and the central BDNF pathway in chronic stress-induced depressive mice through reshaping the gut microbiota.Increasing evidence points to the effect of the gut microbiota on central nervous system functions. Supplementation of certain microbial strains has been demonstrated to alleviate depressive behaviors and neurological abnormalities. This study took the approach to screen for an anti-depressive Bifidobacterium longum strain from fourteen candidates and systematically verified its effect in a chronic stress-induced depression mice model. B. longum subsp. infantis strain CCFM687 could significantly enhance the biosynthesis of 5-hydroxytryptamine (5-HTP) in vitro in RIN14B cells through up-regulation of the Tph1 gene expression. Administration of CCFM687 in mice significantly improved the scores in behavioral tests and increased the level of 5-HTP and serotonin (5-HT) in the prefrontal cortex (PFC) of the brain. The brain-derived neurotrophic factor (BDNF) in the PFC was also increased, possibly through the 5-HT1A-CREB-BDNF pathway. In addition, CCFM687 alleviated the hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis response and accordingly reversed the peripheral inflammation status. Moreover, the stress-induced structural and functional dysbiosis of the gut microbiome was improved by CCFM687, through increased alpha diversity and abundance of butyrate-producing bacteria, in conjunction with inhibition of pathogenic gene expression. In summary, these results indicate that supplementation of B. longum subsp. infantis strain CCFM687 may prevent the onset of depression from chronic stress, and RIN14B could serve as an efficient cell model for rapid screening of anti-depressive probiotics.
1077 related Products with: Ingestion of Bifidobacterium longum subspecies infantis strain CCFM687 regulated emotional behavior and the central BDNF pathway in chronic stress-induced depressive mice through reshaping the gut microbiota.FDA Standard Frozen Tissu Pfu DNA Polymerase protei FDA Standard Frozen Tissu Anti beta3 AR Human, Poly Multiple organ tumor tiss Thermal Shaker with cooli FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu MultiGene Gradient therm FDA Standard Frozen Tissu ELISA TEK™ MBM Thermal
#31488789 // Save this To Up
Magnesium and ketamine in the treatment of depression.Depression affects over 121 million people annually worldwide. Relatively low remission rates among depressive patients enforce the search for new therapeutic solutions and an urgent need to develop faster-acting antidepressants with a different mechanism of action occurs. The pathomechanism of depression postulated by the monoamine hypothesis is limited. The results of abnormalities in glutamate and γ-aminobutyric acid (GABA) systems in the brains of people with mood disorders allowed to develop new theories regarding pathophysiology of these disorders. Glutamatergic transmission is influenced by magnesium and ketamine through glutamatergic N-methyl-D-aspartate receptor (NMDAR) antagonistic effects. Magnesium and ketamine have a common mechanism of action in the treatment of depression: an increase in GluN2B (NMDAR subunit) expression is related to the administration of both of the agents, as well as inhibition of phosphorylation of eEF2 (eukaryotic elongation factor 2) in cell culture and increase of the expression of BDNF in the hippocampus. Combination of ketamine and magnesium in a normal magnesium level presents a superadditive effect in depression treatment. Analysed substances affect the GABAergic system and have anti-inflammatory effects, which is correlated with their antidepressant effect. The synergistic interaction between the pharmacodynamic activity of magnesium and ketamine may be of particular importance for patients with mood disorders. Further research is needed to determine the relationship between magnesium levels and ketamine treatment response mainly in the attempt to establish if the magnesium supplementation can change ketamine treatment response time or present superadditive effect.
FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu MultiGene Gradient therm Multiple organ tumor tiss FDA Standard Frozen Tissu Thermal Shaker with cooli FDA Standard Frozen Tissu FDA Standard Frozen Tissu Rabbit Anti-IAA (Indole-3 MAP2K6 & RELA Protein Pro Colon adenocarcinoma tiss
#31379619 // Save this To Up
Effects of Aspirin in Rats With Ouabain Intracerebral Treatment-Possible Involvement of Inflammatory Modulation?Bipolar disorder (BD) is a chronic and refractory disease with high probability of morbidity and mortality. Although epidemiological studies have established a strong association between BD and immune dysfunction, the precise etiology is still debatable, and the underpinning mechanism remains poorly investigated and understood. In the present study, manic-like symptoms of BD were induced in rats after intracerebroventricular administration of ouabain. Aspirin, a commonly used anti-inflammatory agent, was used to treat the induced manic-like symptoms and inflammation. Concentrations of a spectrum of inflammatory cytokines were examined by enzyme-linked immunosorbent assay in both plasma and brain tissues, and expression of Toll-like receptors 3 and 4 were determined in rat brains. Locomotor activity was monitored with open-field test to assess the effects of ouabain challenge and to evaluate the treatment efficacy of aspirin. Ouabain administration recapitulated many mania-like features such as increased stereotypic counts, traveling distance in open-field test, and decreased expression of brain-derived neurotrophic factor, interferon gamma, and Toll-like receptor 3, which were frequently found in patients with BD. These abnormalities could be partially reversed by aspirin. Our findings suggest that aspirin could be used as a promising adjunctive therapy for BD.
2211 related Products with: Effects of Aspirin in Rats With Ouabain Intracerebral Treatment-Possible Involvement of Inflammatory Modulation?Human Macrophage Inflamma Mouse Macrophage Inflamma Human Gro g Macrophage In Human Macrophage Inflamma Rat Macrophage Inflammato Human, Allograft Inflamma Mouse Macrophage Inflamma Human Macrophage Inflamma Syringe pump can be contr Human Macrophage Inflamma Mouse Macrophage Inflamma Ofloxacin CAS Number [824
#31359683 // Save this To Up
[Study on mechanism for treating ischemic stroke of Siegesbeckiae Herba based on network pharmacology].Xixiancao( Siegesbeckiae Herba) has the effect of treating ischemic stroke( IS),however,the mechanism has not been fully elucidated. In this study,combined with Lipinski's five principles and Veber oral bioavailability rules,68 chemical components of Xixiancao were obtained by database and literature search. Based on the reverse targeting,248 potential targets were obtained and mapped it to the ischemic stroke target set,47 potential targets for the treatment of ischemic stroke were obtained. Molecular docking technique was used to verify that the Xixiancao component has good binding activity to potential targets. GO enrichment analysis and pathway analysis were performed on potential targets using Clue GO. GO enrichment analysis showed that Xixiancao was mainly involved in life processes such as neuronal apoptosis,cholesterol storage and blood pressure regulation. Pathway analysis showed that Xixiancao may promote vascular repairing and regeneration by regulating the expression of ADAMTS1,FLT1 and KDR in VEGFA-VEGFR2 signaling pathway,activate cell survival signals and inhibit neuronal apoptosis by regulating the expression of CAMK2 AA,MDM2,MAPK1,MAPK3,CDK5 and MAPK10 in brain-derived neurotrophic factor signaling pathway and PI3 K-Akt signaling pathway. Lipid homeostasis and inflammation may also be regulated by Xixiancao through regulating the expression of ESR1,NR1 H3,PPARA,PPARG in the nuclear receptor signaling pathway. In addition,Xixiancao could also prevent platelet aggregation by regulating the expression of ITGA2 B,F2,F10,and ALB,and play an antithrombotic role. The results of this study indicate that Xixiancao plays an important role in the treatment of ischemic stroke mainly through anti-thrombosis,promoting angiogenesis,protecting neurons,anti-inflammatory and regulating blood pressure and lipids.
2540 related Products with: [Study on mechanism for treating ischemic stroke of Siegesbeckiae Herba based on network pharmacology].Benz[j]aceanthrylen-2(1H) c-erbB-2 Oncoprotein Bcl-2 Oncoprotein; Clone Oncostatin M, human recom Ondansetron CAS Number [9 Rabbit Anti-FGF3 Oncogene c-erbB-2 Oncoprotein; Cl Mouse Anti-HPV 16 Oncopro Mouse anti human Oncostat c-erbB-3 Oncoprotein; Cl c-erbB-3 Oncoprotein; Cl Ondasetron CAS: [99614-02
#31354429 // Save this To Up
Activation of β2-Adrenoceptor Attenuates Sepsis-Induced Hippocampus-Dependent Cognitive Impairments by Reversing Neuroinflammation and Synaptic Abnormalities.Sepsis-associated encephalopathy induces cognitive dysfunction via mechanisms that commonly involve neuroinflammation and synaptic plasticity impairment of the hippocampus. The β2-adrenoceptor (β2-AR) is a G-protein coupled receptor that regulates immune response and synaptic plasticity, whereas its dysfunction has been implicated in various neurodegenerative diseases. Thus, we hypothesized abnormal β2-AR signaling is involved in sepsis-induced cognitive impairment. In the present study, C57BL/6 mice were subjected to cecal ligation and puncture (CLP) to mimic the clinical human sepsis-associated encephalopathy. The levels of hippocampal β2-AR, proinflammatory cytokines tumor necrosis factor (TNF-α), interleukin-1β (IL-1β), IL-6, cAMP-response element binding protein (CREB), brain derived neurotrophic factor (BDNF), post-synaptic density protein 95 (PSD95), and NMDA receptor 2 B subtypes (GluN2B) were determined at 6, 12, 24 h and 7 and 16 days after CLP. For the interventional study, mice were treated with β2-AR agonist clenbuterol in two ways: early treatment (immediately following CLP) and delayed treatment (on the 8th day following CLP). Neurobehavioral performances were assessed by open field and fear conditioning tests. Here, we found that hippocampal β2-AR expression was significantly decreased starting from 12 h and persisted until 16 days following CLP. Besides, sepsis mice also exhibited increasing neuroinflammation, down-regulated CREB/BDNF, decreasing PSD95 and GluN2B expression, and displayed hippocampus-dependent cognitive impairments. Notably, early clenbuterol treatment alleviated sepsis-induced cognitive deficits by polarizing microglia toward an anti-inflammatory phenotype, reducing proinflammatory cytokines including IL-1β, TNF-α, and up-regulating CREB/BDNF, PSD95, and GluN2B. Intriguingly, delayed clenbuterol treatment also improved cognitive impairments by normalization of hippocampal CREB/BDNF, PSD95, and GluN2B. In summary, our results support the beneficial effects of both early and delayed clenbuterol treatment, which suggests that activation of β2-AR has a translational value in sepsis-associated organ dysfunction including cognitive impairments.
1899 related Products with: Activation of β2-Adrenoceptor Attenuates Sepsis-Induced Hippocampus-Dependent Cognitive Impairments by Reversing Neuroinflammation and Synaptic Abnormalities.Anti AICDA(Activation ind Anti-AICDA(Activation-ind Rabbit Anti-IEX1 Differen (5α)-Androstane-3,11,17- Rabbit Anti-Rat Androgen Androstane 3a,17b diol Gl OxiSelect™ Cellular UV- Bovine Androstenedione,AS Anti-CACNA1b(Voltage-depe Malic enzyme 2, NAD(+) de to FAPβ (Fibroblast Act Jurkat Cell Extract (Indu
#31271959 // Save this To Up
Design, synthesis and biological evaluation of 3-(imidazo[1,2-a]pyrazin-3-ylethynyl)-2-methylbenzamides as potent and selective pan-tropomyosin receptor kinase (TRK) inhibitors.A series of 3-(imidazo[1,2-a]pyrazin-3-ylethynyl)-2-methylbenzamides was designed and synthesized as new tropomyosin receptor kinases (Trks) inhibitors by utilizing a structure-guided optimization strategy. One of the most potent compounds 9o suppressed TrkA/B/C with IC values of 2.65, 10.47 and 2.95 nM, respectively. The compound dose-dependently inhibited brain-derived neurotrophic factor (BDNF)-mediated TrkB activation and suppressed migration and invasion of SH-SY5Y-TrkB neuroblastoma cells expressing high level of TrkB. Inhibitor 9o also inhibited the proliferation of SH-SY5Y-TrkB cells with an IC value of 58 nM, which was comparable to that of an US FDA recently approved drug LOXO-101. Compound 9o may serve as a new lead compound for further anti-cancer drug discovery.
1904 related Products with: Design, synthesis and biological evaluation of 3-(imidazo[1,2-a]pyrazin-3-ylethynyl)-2-methylbenzamides as potent and selective pan-tropomyosin receptor kinase (TRK) inhibitors.CAR,Car,Constitutive andr Androgen Receptor , Mouse Recombinant Human Androge Androgen Receptor (Phosph Androgen Receptor (Phosph Androgen Receptor Antibod Anti Androgen Receptor pr AZD-3514 Mechanisms: Andr Androgen Receptor Goat Anti-Human Androgen Androgen Receptor (Ab-650 CAR,CAR,Constitutive acti
#31265210 // Save this To Up
Effects of VEGF inhibitors on human retinal pigment epithelium under high glucose and hypoxia.Retinal pigment epithelium (RPE) is known to secrete factors important for retinal homeostasis. How this secretome changes in diabetic eyes treated with anti-vascular endothelial growth factor (VEGF) inhibitors is unclear.
2898 related Products with: Effects of VEGF inhibitors on human retinal pigment epithelium under high glucose and hypoxia.ELISA Human , Pigment Epi Cytokine (Human) Antibody Recombinant Human VEGF-C Rabbit anti VEGFR-2 KDR ( Recombinant Human FLT4 VE Inflammation (Human) Anti Recombinant Human VEGF VE Human VEGF-D Premade Aden Human Vascular Endothelia VEGF-C, human recombinant Human Vascular Endothelia Recombinant Human VEGFB P
#31250384 // Save this To Up
Neurotrophic Factors Mediated Activation of Astrocytes Ameliorate Memory Loss by Amyloid Clearance after Transplantation of Lineage Negative Stem Cells.Alzheimer's disease (AD) is one of the untreatable neurodegenerative disorders with associated societal burden. Current therapies only provide symptomatic relief without altering the rate of disease progression as reported by Lanctot et al. (Therapeutic Advances in Neurological Disorders 2 (3):163-180, 2009). The increased number of failed clinical trials in last two decades indicates the imperative need to explore alternative therapies for AD as reported by Tuszynski et al. (Nature Medicine 11 (5):551-555, 2005) and Liyanage et al. (Alzheimer's & Dementia 4:628-635, 2005). In this study, we aimed to decipher the role of neurotrophic factors in the reversal of memory loss by transplantation of lineage negative (Lin-ve) stem cells in a male mouse model of cognitive impairment induced by intrahippocampal injection of amyloid β-42 (Aβ-42). The efficacy of human umbilical cord blood (hUCB) derived Lin-ve stem cells were analyzed by neurobehavioral parameters, i.e., Morris water maze and passive avoidance after bilateral intra-hippocampal transplantation using stereotaxic surgery. Real-time PCR and immunohistochemistry was carried out in brain tissues in order to analyze the expression of neurotrophic factors, apoptotic, astrocytic, and other neuronal cell markers. The transplantation of Lin-ve stem cells led to reversal of memory loss associated with reduction of Aβ-42 deposition from the brains. The molecular analysis revealed increase in neurotrophic factors, i.e., glial derived neurotrophic factor (GDNF), ciliary derived neurotrophic factor (CNTF), and Brain-derived neurotrophic factor (BDNF) after transplantation. The administration of ANA-12, a TrkB inhibitor, reversed the behavioral and molecular effects of stem cell transplantation suggesting involvement of BDNF-TrkB pathway in the rescue of memory loss. We believe that the amyloid clearance results from activation of astrocytes and anti-apoptotic pathways added by neurotrophic factors.
1019 related Products with: Neurotrophic Factors Mediated Activation of Astrocytes Ameliorate Memory Loss by Amyloid Clearance after Transplantation of Lineage Negative Stem Cells.Transcription factors: O Rat Mesenchymal Stem Cell Macrophage Colony Stimula Stem Cell TF Activation P Ofloxacin CAS Number [824 129 Mouse Embryonic Stem Stemez hN2 Human Neuron D Macrophage Colony Stimula Human Synovial Microvascu Mouse IgG2b Negative Cont Contact Factors: Human co Human Amyloid Beta Precur
#31173966 // Save this To Up
Pharmacokinetics of oral and intravenous cannabidiol and its antidepressant-like effects in chronic mild stress mouse model.Cannabidiol (CBD) exhibits significant efficacy in mental and inflammatory diseases. Several studies have recently reported on the rapid antidepressant-like effects of CBD, suggesting that CBD is a potential anti-depressant or anti-stress drug. However, CBD is mainly administered orally or by inhalation with poor bioavailability, resulting in high costs. We aim to explore the efficacy of long-term periodic administration of CBD in chronic mild stress (CMS) via two routes and its pharmacokinetics. We treated ICR mice with CBD administered orally and intravenously and then determined the kinetic constants. A single bolus intravenous injection of CBD resulted in a half-life of 3.9 h, mean residence time of 3.3 h, and oral bioavailability of about 8.6%. The antidepressant-like effects of periodically administered CBD on the chronic mild stress mouse model are evaluated. Results demonstrated that such treatment at a high dose of 100 mg/kg CBD (p.o.) or a low dose of 10 mg/kg CBD (i.v.), elicited significant antidepressant-like behavioral effects in forced swim test, following increased mRNA expression of brain-derived neurotrophic factor (BDNF) and synaptophysin in the prefrontal cortex and the hippocampus. Our findings are expected to provide a reference for the development of intravenous antidepressant formulations of CBD.
1691 related Products with: Pharmacokinetics of oral and intravenous cannabidiol and its antidepressant-like effects in chronic mild stress mouse model.CAR,Car,Constitutive andr Androgen Receptor , Mouse Androgen Receptor , Mouse Goat Anti-Mouse ADRA2A, ( Goat Anti-Mouse, Rat GPR9 Androgen Receptor Antibod Mouse Anti-Insulin-Like G Goat Anti-Human, Mouse, R Rat monoclonal anti mouse Mouse Anti-Influenza A Vi Goat Anti-Human Androgen DMPO, N1664A Host Mouse S
#31127002 // Save this To Up
Neuromodulatory Action of Picomolar Extracellular Aβ42 Oligomers on Presynaptic and Postsynaptic Mechanisms Underlying Synaptic Function and Memory.Failure of anti-amyloid-β peptide (Aβ) therapies against Alzheimer's disease (AD), a neurodegenerative disorder characterized by high amounts of the peptide in the brain, raised the question of the physiological role of Aβ released at low concentrations in the healthy brain. To address this question, we studied the presynaptic and postsynaptic mechanisms underlying the neuromodulatory action of picomolar amounts of oligomeric Aβ (oAβ) on synaptic glutamatergic function in male and female mice. We found that 200 pm oAβ induces an increase of frequency of miniature EPSCs and a decrease of paired pulse facilitation, associated with an increase in docked vesicle number, indicating that it augments neurotransmitter release at presynaptic level. oAβ also produced postsynaptic changes as shown by an increased length of postsynaptic density, accompanied by an increased expression of plasticity-related proteins such as cAMP-responsive element binding protein phosphorylated at Ser133, calcium-calmodulin-dependent kinase II phosphorylated at Thr286, and brain-derived neurotrophic factor, suggesting a role for Aβ in synaptic tagging. These changes resulted in the conversion of early into late long-term potentiation through the nitric oxide/cGMP/protein kinase G intracellular cascade consistent with a cGMP-dependent switch from short- to long-term memory observed after intrahippocampal administration of picomolar amounts of oAβ These effects were present upon extracellular but not intracellular application of the peptide and involved α7 nicotinic acetylcholine receptors. These observations clarified the physiological role of oAβ in synaptic function and memory formation providing solid fundamentals for investigating the pathological effects of high Aβ levels in the AD brains. High levels of oligomeric amyloid-β (oAβ) induce synaptic dysfunction leading to memory impairment in Alzheimer's disease (AD). However, at picomolar concentrations, the peptide is needed to ensure long-term potentiation (LTP) and memory. Here, we show that extracellular 200 pm oAβ concentrations increase neurotransmitter release, number of docked vesicles, postsynaptic density length, and expression of plasticity-related proteins leading to the conversion of early LTP into late LTP and of short-term memory into long-term memory. These effects require α7 nicotinic acetylcholine receptors and are mediated through the nitric oxide/cGMP/protein kinase G pathway. The knowledge of Aβ function in the healthy brain might be useful to understand the causes leading to its increase and detrimental effect in AD.
1741 related Products with: Neuromodulatory Action of Picomolar Extracellular Aβ42 Oligomers on Presynaptic and Postsynaptic Mechanisms Underlying Synaptic Function and Memory.AZD-3514 Mechanisms: Andr CAR,CAR,Constitutive acti Androgen Receptor (Ab 650 ∆2-Androstene-1α,17β- Androstenedione 19 Anti-Androgen Receptor pr Androgen Receptor Ab-1 An Andrographolide C20H30O5 rac Androst-16-en-2,2,5,6 3-O-Acetyl 5,14-Androstad Rabbit Anti-Human Androge Recombinant Human Androge
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