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  • 97
    Millipore lps
    TNFR-Fc produced a beneficial effect for <t>ALI</t> mice. <t>LPS</t> treatment induced pulmonary vascular leakage. Protein concentrations in BALF was noticeably reduced in TNFR-Fc pretreated mice (N = 3 in each group).
    Lps, supplied by Millipore, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/lps/product/Millipore
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    97
    Millipore lps induced inflammation
    TNFR-Fc produced a beneficial effect for <t>ALI</t> mice. <t>LPS</t> treatment induced pulmonary vascular leakage. Protein concentrations in BALF was noticeably reduced in TNFR-Fc pretreated mice (N = 3 in each group).
    Lps Induced Inflammation, supplied by Millipore, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/lps induced inflammation/product/Millipore
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    99
    Millipore lps induced pneumonitis
    TNFR-Fc produced a beneficial effect for <t>ALI</t> mice. <t>LPS</t> treatment induced pulmonary vascular leakage. Protein concentrations in BALF was noticeably reduced in TNFR-Fc pretreated mice (N = 3 in each group).
    Lps Induced Pneumonitis, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/lps induced pneumonitis/product/Millipore
    Average 99 stars, based on 1 article reviews
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    lps induced pneumonitis - by Bioz Stars, 2021-03
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    97
    SAS institute lps induced inflammation model
    Effects of cytochrome P450 inhibitors (CYPI) on the antidepressant effects and pharmacokinetic profiles of ( R )-ketamine (( R )-Ket) in the <t>lipopolysaccharide</t> <t>(LPS)-induced</t> inflammation model. a Experimental schedules for the pharmacokinetic studies following the intraperitoneal administration of ( R )-Ket. b – d Plasma concentration–time profiles of ( R )-Ket, ( R )-norketamine (( R )-NK), and (2 R ,6 R )-hydroxynorketamine ((2 R ,6 R <t>)-HNK)</t> after the administration of ( R )-Ket (3 mg/kg) without ( b ) and with ( c ) CYPI pretreatment, and ( R )-Ket (10 mg/kg) without CYPI pretreatment ( d ). Following the administration of ( R )-Ket, blood was collected sequentially at 5, 15, and 30 min and at 1, 2, and 3 h from the tail vein of each individual mouse. e , f Effect of CYPI pretreatment on the plasma maximum concentration ( C max ; e ) and the area under the concentration–time curve from time 0 to 3 h (AUC 0-3h ; F) of ( R )-Ket, ( R )-NK, and (2 R ,6 R )-HNK. Pretreatment with CYPI completely blocked (2 R ,6 R )-HNK formation to below the lower limit of quantification (BLQ;
    Lps Induced Inflammation Model, supplied by SAS institute, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/lps induced inflammation model/product/SAS institute
    Average 97 stars, based on 1 article reviews
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    lps induced inflammation model - by Bioz Stars, 2021-03
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    N/A
    Lipopolysaccharide Induced Tnf Factor Antibody is a Rabbit Polyclonal antibody against Lipopolysaccharide Induced Tnf Factor
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    N/A
    Lipopolysaccharide Induced TNF Factor Human Recombinant 20 ug
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    Image Search Results


    TNFR-Fc produced a beneficial effect for ALI mice. LPS treatment induced pulmonary vascular leakage. Protein concentrations in BALF was noticeably reduced in TNFR-Fc pretreated mice (N = 3 in each group).

    Journal: PLoS ONE

    Article Title: Inhibition of Acute Lung Injury by TNFR-Fc through Regulation of an Inflammation-Oxidative Stress Pathway

    doi: 10.1371/journal.pone.0151672

    Figure Lengend Snippet: TNFR-Fc produced a beneficial effect for ALI mice. LPS treatment induced pulmonary vascular leakage. Protein concentrations in BALF was noticeably reduced in TNFR-Fc pretreated mice (N = 3 in each group).

    Article Snippet: To generate ALI mouse models, LPS (E. coli O55:B5, 5mg/Kg, Sigma, St. Louis, MO, USA) was intratracheally administered in 50 μL saline.

    Techniques: Produced, Mouse Assay

    Concentration of TNF-α, IL-6, and IL-10 in serum and BALF after LPS/saline injection. Increase in TNF-α and IL-6 from baseline in serum/BALF obtained from mice in response to LPS or TNFR-Fc + LPS. TNFR-Fc decreased serum/BALF TNF-α and IL-6 levels in ALI mice. Serum IL-10 concentration increased after LPS injection. TNFR-Fc increased serum IL-10 in ALI mice. (A) TNF-α, (B) IL-6, (C) IL-10. Error bars represent SEM (N = 3 in each group). * P

    Journal: PLoS ONE

    Article Title: Inhibition of Acute Lung Injury by TNFR-Fc through Regulation of an Inflammation-Oxidative Stress Pathway

    doi: 10.1371/journal.pone.0151672

    Figure Lengend Snippet: Concentration of TNF-α, IL-6, and IL-10 in serum and BALF after LPS/saline injection. Increase in TNF-α and IL-6 from baseline in serum/BALF obtained from mice in response to LPS or TNFR-Fc + LPS. TNFR-Fc decreased serum/BALF TNF-α and IL-6 levels in ALI mice. Serum IL-10 concentration increased after LPS injection. TNFR-Fc increased serum IL-10 in ALI mice. (A) TNF-α, (B) IL-6, (C) IL-10. Error bars represent SEM (N = 3 in each group). * P

    Article Snippet: To generate ALI mouse models, LPS (E. coli O55:B5, 5mg/Kg, Sigma, St. Louis, MO, USA) was intratracheally administered in 50 μL saline.

    Techniques: Concentration Assay, Injection, Mouse Assay

    TNFR-Fc pretreatment depresses TNF-α expression via NF-κB feedback. (A)EMSA for NF-κB binding in lung control nuclear extracts, LPS, and TNFR-Fc + LPS mice (N = 3 in each group). LPS administration caused a marked increase in NF-κB binding to biotin-labeled oligonucleotide probes derived from the TNF-α promoter, and TNFR-Fc pretreatment partially inhibited NF-κB binding. (B)qRT-PCR was used to detect TNF-α mRNA expression (N = 3 in each group). LPS challenge raised TNF-α mRNA expression in ALI mice, and TNFR-Fc pretreatment attenuated TNF-α mRNA transcription. Error bars represent SEM. * P

    Journal: PLoS ONE

    Article Title: Inhibition of Acute Lung Injury by TNFR-Fc through Regulation of an Inflammation-Oxidative Stress Pathway

    doi: 10.1371/journal.pone.0151672

    Figure Lengend Snippet: TNFR-Fc pretreatment depresses TNF-α expression via NF-κB feedback. (A)EMSA for NF-κB binding in lung control nuclear extracts, LPS, and TNFR-Fc + LPS mice (N = 3 in each group). LPS administration caused a marked increase in NF-κB binding to biotin-labeled oligonucleotide probes derived from the TNF-α promoter, and TNFR-Fc pretreatment partially inhibited NF-κB binding. (B)qRT-PCR was used to detect TNF-α mRNA expression (N = 3 in each group). LPS challenge raised TNF-α mRNA expression in ALI mice, and TNFR-Fc pretreatment attenuated TNF-α mRNA transcription. Error bars represent SEM. * P

    Article Snippet: To generate ALI mouse models, LPS (E. coli O55:B5, 5mg/Kg, Sigma, St. Louis, MO, USA) was intratracheally administered in 50 μL saline.

    Techniques: Expressing, Binding Assay, Mouse Assay, Labeling, Derivative Assay, Polymerase Chain Reaction

    TNFR-Fc attenuates lung destruction induced by LPS injection (x200). Representative hematoxylin and eosin-stained preparations of lung tissue from mice 2 h after LPS/saline treatment (N = 3 in each group). (A) Saline-treated mice display regular lung histology. (B) LPS-treated mice displayed typical signs of congestion and disruption of alveolar architecture. (C) TNFR-Fc-pretreated ALI mice were largely protected from these alterations. (D)Histological assessment of the effect TNFR-Fc on LPS-induced lung inflammation and injury (N = 3 in each group). TNFR-Fc pretreatment decreased the ALI score in ALI mice.

    Journal: PLoS ONE

    Article Title: Inhibition of Acute Lung Injury by TNFR-Fc through Regulation of an Inflammation-Oxidative Stress Pathway

    doi: 10.1371/journal.pone.0151672

    Figure Lengend Snippet: TNFR-Fc attenuates lung destruction induced by LPS injection (x200). Representative hematoxylin and eosin-stained preparations of lung tissue from mice 2 h after LPS/saline treatment (N = 3 in each group). (A) Saline-treated mice display regular lung histology. (B) LPS-treated mice displayed typical signs of congestion and disruption of alveolar architecture. (C) TNFR-Fc-pretreated ALI mice were largely protected from these alterations. (D)Histological assessment of the effect TNFR-Fc on LPS-induced lung inflammation and injury (N = 3 in each group). TNFR-Fc pretreatment decreased the ALI score in ALI mice.

    Article Snippet: To generate ALI mouse models, LPS (E. coli O55:B5, 5mg/Kg, Sigma, St. Louis, MO, USA) was intratracheally administered in 50 μL saline.

    Techniques: Injection, Staining, Mouse Assay

    Effects of cytochrome P450 inhibitors (CYPI) on the antidepressant effects and pharmacokinetic profiles of ( R )-ketamine (( R )-Ket) in the lipopolysaccharide (LPS)-induced inflammation model. a Experimental schedules for the pharmacokinetic studies following the intraperitoneal administration of ( R )-Ket. b – d Plasma concentration–time profiles of ( R )-Ket, ( R )-norketamine (( R )-NK), and (2 R ,6 R )-hydroxynorketamine ((2 R ,6 R )-HNK) after the administration of ( R )-Ket (3 mg/kg) without ( b ) and with ( c ) CYPI pretreatment, and ( R )-Ket (10 mg/kg) without CYPI pretreatment ( d ). Following the administration of ( R )-Ket, blood was collected sequentially at 5, 15, and 30 min and at 1, 2, and 3 h from the tail vein of each individual mouse. e , f Effect of CYPI pretreatment on the plasma maximum concentration ( C max ; e ) and the area under the concentration–time curve from time 0 to 3 h (AUC 0-3h ; F) of ( R )-Ket, ( R )-NK, and (2 R ,6 R )-HNK. Pretreatment with CYPI completely blocked (2 R ,6 R )-HNK formation to below the lower limit of quantification (BLQ;

    Journal: Neuropsychopharmacology

    Article Title: (2R,6R)-Hydroxynorketamine is not essential for the antidepressant actions of (R)-ketamine in mice

    doi: 10.1038/s41386-018-0084-y

    Figure Lengend Snippet: Effects of cytochrome P450 inhibitors (CYPI) on the antidepressant effects and pharmacokinetic profiles of ( R )-ketamine (( R )-Ket) in the lipopolysaccharide (LPS)-induced inflammation model. a Experimental schedules for the pharmacokinetic studies following the intraperitoneal administration of ( R )-Ket. b – d Plasma concentration–time profiles of ( R )-Ket, ( R )-norketamine (( R )-NK), and (2 R ,6 R )-hydroxynorketamine ((2 R ,6 R )-HNK) after the administration of ( R )-Ket (3 mg/kg) without ( b ) and with ( c ) CYPI pretreatment, and ( R )-Ket (10 mg/kg) without CYPI pretreatment ( d ). Following the administration of ( R )-Ket, blood was collected sequentially at 5, 15, and 30 min and at 1, 2, and 3 h from the tail vein of each individual mouse. e , f Effect of CYPI pretreatment on the plasma maximum concentration ( C max ; e ) and the area under the concentration–time curve from time 0 to 3 h (AUC 0-3h ; F) of ( R )-Ket, ( R )-NK, and (2 R ,6 R )-HNK. Pretreatment with CYPI completely blocked (2 R ,6 R )-HNK formation to below the lower limit of quantification (BLQ;

    Article Snippet: The effects of ( R )-ketamine, ( R )-norketamine, and (2 R ,6 R )-HNK at 3 h after administration were investigated in the LPS-induced inflammation model.

    Techniques: Concentration Assay

    Effects of ( R )-ketamine (( R )-Ket), ( R )-norketamine (( R )-NK), and (2 R ,6 R )-hydroxynorketamine ((2 R ,6 R )-HNK) in the lipopolysaccharide (LPS)-induced inflammation model and the pharmacokinetic profiles of these compounds. a Experimental schedules for the evaluation of the pharmacological effects of ( R )-Ket, ( R )-NK, and (2 R ,6 R )-HNK. The compounds were administered intraperitoneally (i.p.). b Effects of ( R )-Ket, ( R )-NK, and (2 R ,6 R )-HNK on the LPS-induced increase in the immobility time during the forced swimming test (FST; one-way analysis of variance, F 4,35 = 5.553, P = 0.001). c Effects of ( R )-Ket, ( R )-NK, and (2 R ,6 R )-HNK in the locomotion test (LMT; F 4,35 = 0.356, P = 0.838). b , c Data are represented as the mean ± SEM ( n = 8/group). ** P

    Journal: Neuropsychopharmacology

    Article Title: (2R,6R)-Hydroxynorketamine is not essential for the antidepressant actions of (R)-ketamine in mice

    doi: 10.1038/s41386-018-0084-y

    Figure Lengend Snippet: Effects of ( R )-ketamine (( R )-Ket), ( R )-norketamine (( R )-NK), and (2 R ,6 R )-hydroxynorketamine ((2 R ,6 R )-HNK) in the lipopolysaccharide (LPS)-induced inflammation model and the pharmacokinetic profiles of these compounds. a Experimental schedules for the evaluation of the pharmacological effects of ( R )-Ket, ( R )-NK, and (2 R ,6 R )-HNK. The compounds were administered intraperitoneally (i.p.). b Effects of ( R )-Ket, ( R )-NK, and (2 R ,6 R )-HNK on the LPS-induced increase in the immobility time during the forced swimming test (FST; one-way analysis of variance, F 4,35 = 5.553, P = 0.001). c Effects of ( R )-Ket, ( R )-NK, and (2 R ,6 R )-HNK in the locomotion test (LMT; F 4,35 = 0.356, P = 0.838). b , c Data are represented as the mean ± SEM ( n = 8/group). ** P

    Article Snippet: The effects of ( R )-ketamine, ( R )-norketamine, and (2 R ,6 R )-HNK at 3 h after administration were investigated in the LPS-induced inflammation model.

    Techniques: