p38 mapk activation inhibitor (Biomol GmbH)

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Biomol GmbH p38 mapk activation inhibitor

0.7% ISO reduces ZY-induced <t>p38</t> <t>MAPK</t> activation; p38 MAPK signaling is essential to ZY-induced NF- κ B activation and COX2/PGE 2 generation in vitro . (a) At 0.5 h after ZY or CM (Ctrl) treatment, KCs (1 × 10 6 cells/well in six-well culture plates) were exposed to RA with or without 0.7% ISO for 0.5 h. The cells were continuously stimulated with Ctrl for 0 h and 6 h or ZY (0.5 mg/mL) for 0.5, 1, 2, 3, and 6 h. Western blot analysis was used to assess the phosphorylation of p38 MAPK (Thr180/Tyr182), JNK (Thr183/Tyr185), and ERK1/2 (Thr185/Tyr187). β -Actin was used as the internal control. The ratio from p-p38 MAPK to p38 MAPK is indicated above the bands. (b) The KCs with or without SB202190 (10 μ M) pretreatment for 0.5 h were treated with ZY (0.5 mg/mL) or Ctrl for 1 h. Western blot was performed to determine the phosphorylation of IKK β (Ser180). β -Actin was used as the internal control. The ratio from pIKK β to IKK β is indicated above the bands. (c) The KCs with or without SB202190 (10 μ M) pretreatment for 0.5 h were treated with ZY (0.5 mg/mL) or Ctrl for 24 h. RIA was performed to detect PGE 2 release. Representative data are from three independent experiments and expressed as mean ± SD. * P

P38 Mapk Activation Inhibitor, supplied by Biomol GmbH, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 86 stars, based on 1 article reviews
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p38 mapk activation inhibitor - by Bioz Stars, 2021-04

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1) Product Images from "Subanesthetic Isoflurane Reduces Zymosan-Induced Inflammation in Murine Kupffer Cells by Inhibiting ROS-Activated p38 MAPK/NF-κB Signaling"

Article Title: Subanesthetic Isoflurane Reduces Zymosan-Induced Inflammation in Murine Kupffer Cells by Inhibiting ROS-Activated p38 MAPK/NF-κB Signaling

Journal: Oxidative Medicine and Cellular Longevity

doi: 10.1155/2014/851692

0.7% ISO reduces ZY-induced p38 MAPK activation; p38 MAPK signaling is essential to ZY-induced NF- κ B activation and COX2/PGE 2 generation in vitro . (a) At 0.5 h after ZY or CM (Ctrl) treatment, KCs (1 × 10 6 cells/well in six-well culture plates) were exposed to RA with or without 0.7% ISO for 0.5 h. The cells were continuously stimulated with Ctrl for 0 h and 6 h or ZY (0.5 mg/mL) for 0.5, 1, 2, 3, and 6 h. Western blot analysis was used to assess the phosphorylation of p38 MAPK (Thr180/Tyr182), JNK (Thr183/Tyr185), and ERK1/2 (Thr185/Tyr187). β -Actin was used as the internal control. The ratio from p-p38 MAPK to p38 MAPK is indicated above the bands. (b) The KCs with or without SB202190 (10 μ M) pretreatment for 0.5 h were treated with ZY (0.5 mg/mL) or Ctrl for 1 h. Western blot was performed to determine the phosphorylation of IKK β (Ser180). β -Actin was used as the internal control. The ratio from pIKK β to IKK β is indicated above the bands. (c) The KCs with or without SB202190 (10 μ M) pretreatment for 0.5 h were treated with ZY (0.5 mg/mL) or Ctrl for 24 h. RIA was performed to detect PGE 2 release. Representative data are from three independent experiments and expressed as mean ± SD. * P

Figure Legend Snippet: 0.7% ISO reduces ZY-induced p38 MAPK activation; p38 MAPK signaling is essential to ZY-induced NF- κ B activation and COX2/PGE 2 generation in vitro . (a) At 0.5 h after ZY or CM (Ctrl) treatment, KCs (1 × 10 6 cells/well in six-well culture plates) were exposed to RA with or without 0.7% ISO for 0.5 h. The cells were continuously stimulated with Ctrl for 0 h and 6 h or ZY (0.5 mg/mL) for 0.5, 1, 2, 3, and 6 h. Western blot analysis was used to assess the phosphorylation of p38 MAPK (Thr180/Tyr182), JNK (Thr183/Tyr185), and ERK1/2 (Thr185/Tyr187). β -Actin was used as the internal control. The ratio from p-p38 MAPK to p38 MAPK is indicated above the bands. (b) The KCs with or without SB202190 (10 μ M) pretreatment for 0.5 h were treated with ZY (0.5 mg/mL) or Ctrl for 1 h. Western blot was performed to determine the phosphorylation of IKK β (Ser180). β -Actin was used as the internal control. The ratio from pIKK β to IKK β is indicated above the bands. (c) The KCs with or without SB202190 (10 μ M) pretreatment for 0.5 h were treated with ZY (0.5 mg/mL) or Ctrl for 24 h. RIA was performed to detect PGE 2 release. Representative data are from three independent experiments and expressed as mean ± SD. * P

Techniques Used: Activation Assay, In Vitro, Western Blot

0.7% ISO reduces ZY-induced ROS generation; ROS is essential to ZY-induced activation of p38 MAPK and NF- κ B, as well as PGE 2 production. (a) At 0.5 h after KCs (1 × 10 6 cells/well in six-well culture plates) were treated with ZY or CM (Ctrl) for 0.5 h with or without MCI-186 (50 μ M) pretreatment for 0.5 h, the cells were exposed to RA with or without 0.7% ISO for another 0.5 h. The KCs were continuously treated with ZY (0.5 mg/mL) or Ctrl for 24 h. RIA was performed to detect PGE 2 production. (b) The KCs with or without MCI-186 (50 μ M) pretreatment for 0.5 h were treated with ZY (0.5 mg/mL) or Ctrl for 1 h. Western blot was performed to determine the phosphorylation of p38 MAPK (Thr180/Tyr182) and NF- κ B (Ser536). β -Actin and lamin B were used as the internal controls. The ratios from p-p38 MAPK to p38 MAPK and from pNF- κ B to NF- κ B are indicated above the bands. (c) The KCs (5 × 10 4 cells/well in 96-well culture plates) with or without MCI-186 (50 μ M) pretreatment for 0.5 h were stimulated with ZY (0.5 mg/mL) for 1 h with or without 0.7% ISO posttreatment for 0.5 h. DCFH-DA was used to assess the production of intracellular ROS. Representative data are from three independent experiments and expressed as mean ± SD. * P

Figure Legend Snippet: 0.7% ISO reduces ZY-induced ROS generation; ROS is essential to ZY-induced activation of p38 MAPK and NF- κ B, as well as PGE 2 production. (a) At 0.5 h after KCs (1 × 10 6 cells/well in six-well culture plates) were treated with ZY or CM (Ctrl) for 0.5 h with or without MCI-186 (50 μ M) pretreatment for 0.5 h, the cells were exposed to RA with or without 0.7% ISO for another 0.5 h. The KCs were continuously treated with ZY (0.5 mg/mL) or Ctrl for 24 h. RIA was performed to detect PGE 2 production. (b) The KCs with or without MCI-186 (50 μ M) pretreatment for 0.5 h were treated with ZY (0.5 mg/mL) or Ctrl for 1 h. Western blot was performed to determine the phosphorylation of p38 MAPK (Thr180/Tyr182) and NF- κ B (Ser536). β -Actin and lamin B were used as the internal controls. The ratios from p-p38 MAPK to p38 MAPK and from pNF- κ B to NF- κ B are indicated above the bands. (c) The KCs (5 × 10 4 cells/well in 96-well culture plates) with or without MCI-186 (50 μ M) pretreatment for 0.5 h were stimulated with ZY (0.5 mg/mL) for 1 h with or without 0.7% ISO posttreatment for 0.5 h. DCFH-DA was used to assess the production of intracellular ROS. Representative data are from three independent experiments and expressed as mean ± SD. * P

Techniques Used: Activation Assay, Western Blot

2) Product Images from "Subanesthetic isoflurane abates ROS-activated MAPK/NF-κB signaling to repress ischemia-induced microglia inflammation and brain injury"

Article Title: Subanesthetic isoflurane abates ROS-activated MAPK/NF-κB signaling to repress ischemia-induced microglia inflammation and brain injury

Journal: Aging (Albany NY)

doi: 10.18632/aging.202349

Sub-anesthetic ISO post-conditioning hinders OGD-caused activation of p38 MAPK and NF-κB p65 in microglial cells in co-cultures. ( A ) At the end of 3 h-OGD or Ctrl treatment, co-cultures were exposed to RA with or without 0.7% ISO for 30 min. All the cells were continuously cultured under normal conditions for 6 h after OGD exposure. Then, microglial cells were collected for further analyses. Representative western blots show protein expressions of p-p38 MAPK (Thr180/Tyr182), p38 MAPK, p-JNK1/2 (Thr183/Tyr185), JNK1/2, p-ERK1/2 (Thr185/Tyr187), and ERK1/2. β-actin was used as the internal control. ( B – D ) Co-cultures with or without SB202190 (10 μM) pretreatment for 30 min were subjected to 3 h-OGD or Ctrl treatment and continuously cultured under normal conditions for 6 or 24 h after OGD stimulation. Then, microglial cells were collected for further analyses. ( B ) Representative western blots show total and phosphorylated IKKβ levels at 6 h after OGD exposure. β-actin was used as the internal control. ( C ) Quantification of PGE 2 levels by RIA at 24 h after OGD treatment. ( D ) Quantification of NO production by Griess reagent at 24 h after OGD challenge. Representative data are from three independent experiments and expressed as mean ± SD. Statistical significance: * P

Figure Legend Snippet: Sub-anesthetic ISO post-conditioning hinders OGD-caused activation of p38 MAPK and NF-κB p65 in microglial cells in co-cultures. ( A ) At the end of 3 h-OGD or Ctrl treatment, co-cultures were exposed to RA with or without 0.7% ISO for 30 min. All the cells were continuously cultured under normal conditions for 6 h after OGD exposure. Then, microglial cells were collected for further analyses. Representative western blots show protein expressions of p-p38 MAPK (Thr180/Tyr182), p38 MAPK, p-JNK1/2 (Thr183/Tyr185), JNK1/2, p-ERK1/2 (Thr185/Tyr187), and ERK1/2. β-actin was used as the internal control. ( B – D ) Co-cultures with or without SB202190 (10 μM) pretreatment for 30 min were subjected to 3 h-OGD or Ctrl treatment and continuously cultured under normal conditions for 6 or 24 h after OGD stimulation. Then, microglial cells were collected for further analyses. ( B ) Representative western blots show total and phosphorylated IKKβ levels at 6 h after OGD exposure. β-actin was used as the internal control. ( C ) Quantification of PGE 2 levels by RIA at 24 h after OGD treatment. ( D ) Quantification of NO production by Griess reagent at 24 h after OGD challenge. Representative data are from three independent experiments and expressed as mean ± SD. Statistical significance: * P

Techniques Used: Activation Assay, Cell Culture, Western Blot

$Sub-anesthetic ISO post-conditioning attenuates MCAO-induced inflammation and apoptosis in rat brains. Rats were subjected to a right MCAO or sham operation (control) for 2 h and then treated with or without 0.7% ISO for 1 h. At 24 h after MCAO, seventy-six rats (Ctrl + RA, n = 20; Ctrl + ISO, n = 20; MCAO + RA, n = 17; MCAO + ISO, n = 19) still survived and then they were sacrificed under anesthesia. ( A ) Representative images of the TTC-stained brain tissue sections showing infarction areas ( n = 8 per group). ( B ) Quantitative measurements of the infraction volume ( n = 8 per group). ( C ) Histogram plots show neurologic deficit scores ( n = 12 per group). ( D ) Quantification of rat serum PGE 2 levels by RIA ( n = 16 per group). ( E ) Quantification of rat serum NO levels by Griess reagent ( n = 16 per group). ( F ) ELISA analysis of the rat serum IL-6 levels ( n = 8 per group). ( G ) Analysis of ROS level by DCFH-DA assay in brain homogenates ( n = 9 per group). The data represent the relative DCF fluorescence. ( H ) Representative western blots show total and phospho-p38 MAPK in the brain homogenates ( n = 9 per group). β-actin was used as the normal control. ( I ) Estimation of NF-κB p65 DNA-binding activity in brain homogenates using a TransAM NF-κB p65 transcription factor assay ( n = 9 per group). ( J ) Estimation of nucleosomal fragmentation in brain tissues ( n = 9 per group). ( K ) Quantitative measurement of caspase-3 activity ( n = 9 per group). Representative data are from three independent experiments and expressed as mean ± SD. Statistical significance: * P$
Figure Legend Snippet: Sub-anesthetic ISO post-conditioning attenuates MCAO-induced inflammation and apoptosis in rat brains. Rats were subjected to a right MCAO or sham operation (control) for 2 h and then treated with or without 0.7% ISO for 1 h. At 24 h after MCAO, seventy-six rats (Ctrl + RA, n = 20; Ctrl + ISO, n = 20; MCAO + RA, n = 17; MCAO + ISO, n = 19) still survived and then they were sacrificed under anesthesia. ( A ) Representative images of the TTC-stained brain tissue sections showing infarction areas ( n = 8 per group). ( B ) Quantitative measurements of the infraction volume ( n = 8 per group). ( C ) Histogram plots show neurologic deficit scores ( n = 12 per group). ( D ) Quantification of rat serum PGE 2 levels by RIA ( n = 16 per group). ( E ) Quantification of rat serum NO levels by Griess reagent ( n = 16 per group). ( F ) ELISA analysis of the rat serum IL-6 levels ( n = 8 per group). ( G ) Analysis of ROS level by DCFH-DA assay in brain homogenates ( n = 9 per group). The data represent the relative DCF fluorescence. ( H ) Representative western blots show total and phospho-p38 MAPK in the brain homogenates ( n = 9 per group). β-actin was used as the normal control. ( I ) Estimation of NF-κB p65 DNA-binding activity in brain homogenates using a TransAM NF-κB p65 transcription factor assay ( n = 9 per group). ( J ) Estimation of nucleosomal fragmentation in brain tissues ( n = 9 per group). ( K ) Quantitative measurement of caspase-3 activity ( n = 9 per group). Representative data are from three independent experiments and expressed as mean ± SD. Statistical significance: * P

Techniques Used: Staining, Enzyme-linked Immunosorbent Assay, DCFH-DA Assay, Fluorescence, Western Blot, Binding Assay, Activity Assay, Transcription Factor Assay

Sub-anesthetic ISO post-conditioning represses ROS-mediated activation of p38 MAPK/NF-κB signaling in OGD-stimulated microglial cells in co-cultures. ( A ) At the end of 3 h-OGD or Ctrl treatment, co-cultures were exposed to RA with or without 0.7% ISO for 30 min. All the cells were continuously cultured under normal conditions for 24 h after OGD exposure. Then, microglial cells were harvested for further analyses. The images of DCFH-DA-stained microglial cells were taken and ROS levels were calculated. Data represent the relative DCF fluorescence. Scale bar: 5 μm. ( B – D ) Co-cultures with or without NAC (5 mM) pretreatment for 30 min were subjected to 3 h-OGD or Ctrl treatment and continuously cultured under normal conditions for 6 or 24 h after OGD stimulation. Then, microglial cells were harvested for assays. ( B ) Representative western blots show total and phosphorylated p38 MAPK and NF-κB p65 levels at 6 h after OGD exposure. β-actin and lamin B were used as the internal controls. ( C ) Quantification of PGE 2 levels by RIA at 24 h after OGD exposure. ( D ) Quantification of NO production by Griess reagent at 24 h after OGD stimulation. Representative data are from three independent experiments and expressed as mean ± SD. Statistical significance: * P

Figure Legend Snippet: Sub-anesthetic ISO post-conditioning represses ROS-mediated activation of p38 MAPK/NF-κB signaling in OGD-stimulated microglial cells in co-cultures. ( A ) At the end of 3 h-OGD or Ctrl treatment, co-cultures were exposed to RA with or without 0.7% ISO for 30 min. All the cells were continuously cultured under normal conditions for 24 h after OGD exposure. Then, microglial cells were harvested for further analyses. The images of DCFH-DA-stained microglial cells were taken and ROS levels were calculated. Data represent the relative DCF fluorescence. Scale bar: 5 μm. ( B – D ) Co-cultures with or without NAC (5 mM) pretreatment for 30 min were subjected to 3 h-OGD or Ctrl treatment and continuously cultured under normal conditions for 6 or 24 h after OGD stimulation. Then, microglial cells were harvested for assays. ( B ) Representative western blots show total and phosphorylated p38 MAPK and NF-κB p65 levels at 6 h after OGD exposure. β-actin and lamin B were used as the internal controls. ( C ) Quantification of PGE 2 levels by RIA at 24 h after OGD exposure. ( D ) Quantification of NO production by Griess reagent at 24 h after OGD stimulation. Representative data are from three independent experiments and expressed as mean ± SD. Statistical significance: * P

Techniques Used: Activation Assay, Cell Culture, Staining, Fluorescence, Western Blot

other:

Article Title: Ligand-independent signals from angiotensin II type 2 receptor induce apoptosis
Article Snippet: The following antibodies and reagents were generously provided as indicated or purchased: AT2 receptor-selective non-peptide antagonist PD123319 (Research Biochemical International), a specific inhibitor of the MEK kinase, PD98059, 2-(2′-amino-3′-methoxyphenyl)oxanaphthalen-4-one (Biomol); the p38 MAP kinase inhibitor SB203580, 4-(4-fluorophenyl)-2-(4-methylsulfonylphenyl)-5-(4-pyridyl)1H-imidazole (Upstate Bio); the caspase-3 inhibitor, Ac-DEVD-chloro methyl ketone (Calbiochem); anti-phospho p38 MAPK antibody #9211S and anti-p38 MAPK antibody #9102 (New England Biolabs).

Activation Assay:

Article Title: Subanesthetic isoflurane abates ROS-activated MAPK/NF-κB signaling to repress ischemia-induced microglia inflammation and brain injury
Article Snippet: Horseradish peroxidase (HRP)-conjugated anti-rabbit IgG (cat#: 0111-01) was provided by Chemicon (Temecula, CA, USA). .. NF-κB activation inhibitor (NAI; cat#: S1014-67.1) and p38 MAPK activation inhibitor (SB202190; cat#: 152121-30-7) were supplied by Biomol (Plymouth Meeting, PA, USA). .. ROS scavenger (NAC; cat#: A7250) and iNOS activity inhibitor (1400W; cat#: W4262) were purchased from Sigma–Aldrich (St. Louis, MO, USA).

Article Title: Subanesthetic Isoflurane Reduces Zymosan-Induced Inflammation in Murine Kupffer Cells by Inhibiting ROS-Activated p38 MAPK/NF-κB Signaling
Article Snippet: Horseradish peroxidase-conjugated anti-rabbit IgG was obtained from Chemicon (Temecula, CA, USA). .. ROS scavenger (Edaravone, MCI-186) was from Tocris Bioscience (Ellisville, MO, USA). p38 MAPK activation inhibitor (SB202190) and NF-κ B activation inhibitor (NAI) were purchased from Biomol (Plymouth Meeting, PA, USA) and Calbiochem (Darmstadt, Germany), respectively. .. ZY from S. cerevisiae was dissolved in isotonic sodium chloride solution to a final concentration of 25 mg/mL.

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Effect of <t>p38</t> <t>MAPK</t> inhibitor, SB203580 (SB), on SST-induced stimulation of butyrate uptake in Caco-2 cells. Overnight serum-starved postconfluent Caco2 cells were preincubated with SB203580 (30 μM), specific inhibitor of p38 MAPK for 60 min in

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<t>p38</t> <t>MAPK</t> inhibitor and NF-κB inhibitor reduced microbial activation of TL1A expression

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The roles of TLR4 and NF-κB in IL-8 release from OMV-stimulated endothelial cells. (A) Total RNA was isolated from HMEC-1 treated with PBS or E. coli OMVs (0.5 ng/mL) for 12 h, and mRNA expression of TLRs (TLR1–TLR9), MD2, CD14, NOD1, and NOD2 were analyzed by real-time RT-PCR ( n = 3). Fold changes were calculated by dividing the expression of each gene by that of GAPDH. (B) HMEC-1 was treated with E. coli OMVs (0.5 ng/mL in total protein concentration) or TLR agonists for 12 h, and the concentrations of IL-8 were quantified in the culture supernatants by ELISA ( n = 3). Human TLR agonists were used as follows: TLR1/2 agonist, Pam 3 CSK 4 , 100 ng/mL; TLR2/6 agonist, FSL1, 100 ng/mL; TLR2 agonist, HKLM, 10 7 cells/mL; TLR3 agonist, poly (I:C), 1 μg/mL; TLR4 agonist, LPS-EK, 10 ng/mL; TLR5 agonist, FLA-ST, 100 ng/mL; TLR7 agonist, imiquimod, 100 ng/mL; TLR8 agonist, ssRNA40, 10 ng/mL; and TLR9 agonist, ODN2006, 500 nM. (C) PBS, E. coli OMVs (10 ng/mL in total protein concentration), or LPS-EK (10 ng/mL) were treated to HMEC-1, with or without TLR4 antagonist (1 μg/mL) for 12 h, and the concentrations of IL-8 were measured in the culture supernatants by ELISA ( n = 3). (D) Various concentrations (0, 0.01, 0.1, 1, and 10 ng/mL in total protein concentrations) of E. coli W3110 wild-type OMVs or E. coli W3110 ΔmsbB mutant OMVs were treated to HMEC-1 for 12 h, and the concentrations of IL-8 were measured in the culture supernatants by ELISA. (E) PBS or E. coli OMVs (0.5 ng/mL in total protein concentration) were treated to HMEC-1 for 12 h with 0.05% dimethyl sulfoxide (–) or the following signaling inhibitors (final concentration = 10 μM in 0.05% dimethyl sulfoxide): PD98059 (ERK1/2 inhibitor), <t>SB203580</t> (p38 MAPK inhibitor), SP600125 (JNK inhibitor), LY294002 (PI3K inhibitor), and BAY11-7082 (NK-κB inhibitor), and the concentrations of IL-8 were measured in the culture supernatants by ELISA ( n = 3). (F) PBS or E. coli OMVs (0.5 ng/mL in total protein concentration) were treated to HMEC-1 for 12 h with various concentrations of BAY11-7082 (0, 0.1, 1, 5, and 10 μM), and the concentrations of IL-8 were measured in the culture supernatants by ELISA ( n = 3). (G,H) HMEC-1 were treated with PBS or E. coli OMVs (0.5 ng/mL in total protein concentration) for 0, 10, 30, 60, 120, or 360 min. Whole cell lysates (20 μg in total protein amount) were subjected to analyzing the expression of phosphorylated-IκB (P-IκB) and β-actin by Western blot. The representative blot of two independent experiments (G) and the average values of the relative ratios calculated by dividing the densitometry quantification values for P-IκB by those of β-actin (H) . (I) Various concentrations (0, 0.01, 0.1, 1, 10, and 100 ng/mL) of E. coli LPS, OMVs-UC, or OMVs-BDG were treated to HMEC-1 for 12 h, and the concentrations of IL-8 were measured in the culture supernatants by ELISA. LPS, LPS isolated from E. coli ; OMVs-UC, OMVs isolated by the combination of ultrafiltration and ultracentrifugation (UC); OMVs-BDG, OMVs isolated by the combination of ultrafiltration, ultracentrifugation, buoyant density gradient ultracentrifugation (BDG), and ultracentrifugation. (J) Wild-type mice were intraperitoneally administered with PBS, E. coli LPS (11.25 μg per mouse), or E. coli OMVs-UC (15 μg in total protein amounts per mouse) or E. coli OMVs-BDG (15 μg in total protein amounts per mouse). Five mice were used for each group. At 6 h after administration, the mice were killed. The BAL fluids were retrieved, and the concentration of CXCL1 was measured in the BAL fluid by ELISA ( n = 5). Data were represented as mean ± SEM. ns, non-significant; ∗∗ P

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<t>p38-MAPK</t> and ERK pathways in DC polarization. (A, B) Control LPS-mDC (black bars) or DC pre-treated with 25 μM SB203580 (A) or with 40μM PD98059 (B) before addition of LPS at day 6 (grey bars) were cocultured with T cells. Data are shown for 1/20 DC/T cell ratio and were similar for other ratios. Secretions of IFNγ, IL-5 and IL-13 were measured in coculture supernatants at day 5. Cytokine secretion was normalized to 100% for control mDC. Mean ± SD of three independent experiments. (C, D) p38-MAPK inhibitor prevents Th2 polarization of LPS-stimulated DC. Control LPS-stimulated DC (black bars), LPS-stimulated DC pre-treated with 1-MT (opened bars) or LPS-stimulated DC pre-treated with SB203580 and 1-MT (hatched bars) were cultured with T cells. Secretions of IFNγ (C), IL-5 and IL-13 (D) were measured in coculture supernatants at day 5. Cytokine secretion was normalized to 100% for control mDC. Mean ± SD of three independent experiments. (E, F) MEK/ERK pathway inhibitor restores the Th1 polarization of DC treated by 1-MT and LPS. Control LPS-stimulated DC (black bars), LPS-stimulated DC pre-treated with 1-MT (opened bars) or LPS-stimulated DC pre-treated with PD98059 and 1-MT (grey bars) were cultured with T cells. Secretions of IFNγ (E), IL-5 and IL-13 (F) were measured in the supernatants at day 5 of coculture. Cytokine secretion was normalized to 100% for control LPS-stimulated DC. Mean ± SD of three independent experiments.

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Image Search Results

Effect of p38 MAPK inhibitor, SB203580 (SB), on SST-induced stimulation of butyrate uptake in Caco-2 cells. Overnight serum-starved postconfluent Caco2 cells were preincubated with SB203580 (30 μM), specific inhibitor of p38 MAPK for 60 min in

Journal: American Journal of Physiology - Gastrointestinal and Liver Physiology

Article Title: Mechanisms underlying modulation of monocarboxylate transporter 1 (MCT1) by somatostatin in human intestinal epithelial cells

doi: 10.1152/ajpgi.00283.2009

Figure Lengend Snippet: Effect of p38 MAPK inhibitor, SB203580 (SB), on SST-induced stimulation of butyrate uptake in Caco-2 cells. Overnight serum-starved postconfluent Caco2 cells were preincubated with SB203580 (30 μM), specific inhibitor of p38 MAPK for 60 min in

Article Snippet: SST and seglitide were obtained from Sigma (St. Louis, MO). p38 MAPK inhibitor, SB 203580, was obtained from Biomol (Plymouth Meeting, PA).

Techniques:

SST induces MCT1/CD147 association in Caco-2 cells. Overnight serum-starved postconfluent Caco2 cells were treated with SST (25 and 50 nM) in serum-free cell culture medium for 30–60 min. Cells were also pretreated with the p38 MAPK inhibitor

Journal: American Journal of Physiology - Gastrointestinal and Liver Physiology

Article Title: Mechanisms underlying modulation of monocarboxylate transporter 1 (MCT1) by somatostatin in human intestinal epithelial cells

doi: 10.1152/ajpgi.00283.2009

Figure Lengend Snippet: SST induces MCT1/CD147 association in Caco-2 cells. Overnight serum-starved postconfluent Caco2 cells were treated with SST (25 and 50 nM) in serum-free cell culture medium for 30–60 min. Cells were also pretreated with the p38 MAPK inhibitor

Article Snippet: SST and seglitide were obtained from Sigma (St. Louis, MO). p38 MAPK inhibitor, SB 203580, was obtained from Biomol (Plymouth Meeting, PA).

Techniques: Cell Culture

p38 MAPK inhibitor and NF-κB inhibitor reduced microbial activation of TL1A expression

Journal: European journal of immunology

Article Title: Microbial Induction of Inflammatory Bowel Disease Associated Gene TL1A (TNFSF15) in Antigen Presenting Cells

doi: 10.1002/eji.200839087

Figure Lengend Snippet: p38 MAPK inhibitor and NF-κB inhibitor reduced microbial activation of TL1A expression

Article Snippet: For inhibitory experiments, p38 MAPK inhibitors (SB-203580, Biomol, 1μM; SB-239063, Tocris bioscience, 200 nM) and NF-κB inhibitors (MG-132, Biomol, 10 μM; IKK-NBD or IKK-control, 100 γM; QNZ, Biomol, 20 nM) were introduced 15 min prior to the addition of the stimulatory agonists.

Techniques: Activation Assay, Expressing

Induction of TL1A is partly mediated by TLR signaling pathway and dependent on live bacteria, NF-κB and p38 MAPK activity

Journal: European journal of immunology

Article Title: Microbial Induction of Inflammatory Bowel Disease Associated Gene TL1A (TNFSF15) in Antigen Presenting Cells

doi: 10.1002/eji.200839087

Figure Lengend Snippet: Induction of TL1A is partly mediated by TLR signaling pathway and dependent on live bacteria, NF-κB and p38 MAPK activity

Techniques: Activity Assay

Journal: Frontiers in Microbiology

Article Title: Outer Membrane Vesicles Derived From Escherichia coli Regulate Neutrophil Migration by Induction of Endothelial IL-8

doi: 10.3389/fmicb.2018.02268

Figure Lengend Snippet: The roles of TLR4 and NF-κB in IL-8 release from OMV-stimulated endothelial cells. (A) Total RNA was isolated from HMEC-1 treated with PBS or E. coli OMVs (0.5 ng/mL) for 12 h, and mRNA expression of TLRs (TLR1–TLR9), MD2, CD14, NOD1, and NOD2 were analyzed by real-time RT-PCR ( n = 3). Fold changes were calculated by dividing the expression of each gene by that of GAPDH. (B) HMEC-1 was treated with E. coli OMVs (0.5 ng/mL in total protein concentration) or TLR agonists for 12 h, and the concentrations of IL-8 were quantified in the culture supernatants by ELISA ( n = 3). Human TLR agonists were used as follows: TLR1/2 agonist, Pam 3 CSK 4 , 100 ng/mL; TLR2/6 agonist, FSL1, 100 ng/mL; TLR2 agonist, HKLM, 10 7 cells/mL; TLR3 agonist, poly (I:C), 1 μg/mL; TLR4 agonist, LPS-EK, 10 ng/mL; TLR5 agonist, FLA-ST, 100 ng/mL; TLR7 agonist, imiquimod, 100 ng/mL; TLR8 agonist, ssRNA40, 10 ng/mL; and TLR9 agonist, ODN2006, 500 nM. (C) PBS, E. coli OMVs (10 ng/mL in total protein concentration), or LPS-EK (10 ng/mL) were treated to HMEC-1, with or without TLR4 antagonist (1 μg/mL) for 12 h, and the concentrations of IL-8 were measured in the culture supernatants by ELISA ( n = 3). (D) Various concentrations (0, 0.01, 0.1, 1, and 10 ng/mL in total protein concentrations) of E. coli W3110 wild-type OMVs or E. coli W3110 ΔmsbB mutant OMVs were treated to HMEC-1 for 12 h, and the concentrations of IL-8 were measured in the culture supernatants by ELISA. (E) PBS or E. coli OMVs (0.5 ng/mL in total protein concentration) were treated to HMEC-1 for 12 h with 0.05% dimethyl sulfoxide (–) or the following signaling inhibitors (final concentration = 10 μM in 0.05% dimethyl sulfoxide): PD98059 (ERK1/2 inhibitor), SB203580 (p38 MAPK inhibitor), SP600125 (JNK inhibitor), LY294002 (PI3K inhibitor), and BAY11-7082 (NK-κB inhibitor), and the concentrations of IL-8 were measured in the culture supernatants by ELISA ( n = 3). (F) PBS or E. coli OMVs (0.5 ng/mL in total protein concentration) were treated to HMEC-1 for 12 h with various concentrations of BAY11-7082 (0, 0.1, 1, 5, and 10 μM), and the concentrations of IL-8 were measured in the culture supernatants by ELISA ( n = 3). (G,H) HMEC-1 were treated with PBS or E. coli OMVs (0.5 ng/mL in total protein concentration) for 0, 10, 30, 60, 120, or 360 min. Whole cell lysates (20 μg in total protein amount) were subjected to analyzing the expression of phosphorylated-IκB (P-IκB) and β-actin by Western blot. The representative blot of two independent experiments (G) and the average values of the relative ratios calculated by dividing the densitometry quantification values for P-IκB by those of β-actin (H) . (I) Various concentrations (0, 0.01, 0.1, 1, 10, and 100 ng/mL) of E. coli LPS, OMVs-UC, or OMVs-BDG were treated to HMEC-1 for 12 h, and the concentrations of IL-8 were measured in the culture supernatants by ELISA. LPS, LPS isolated from E. coli ; OMVs-UC, OMVs isolated by the combination of ultrafiltration and ultracentrifugation (UC); OMVs-BDG, OMVs isolated by the combination of ultrafiltration, ultracentrifugation, buoyant density gradient ultracentrifugation (BDG), and ultracentrifugation. (J) Wild-type mice were intraperitoneally administered with PBS, E. coli LPS (11.25 μg per mouse), or E. coli OMVs-UC (15 μg in total protein amounts per mouse) or E. coli OMVs-BDG (15 μg in total protein amounts per mouse). Five mice were used for each group. At 6 h after administration, the mice were killed. The BAL fluids were retrieved, and the concentration of CXCL1 was measured in the BAL fluid by ELISA ( n = 5). Data were represented as mean ± SEM. ns, non-significant; ∗∗ P

Article Snippet: The signaling inhibitors were PD98059 (ERK1/2 inhibitor), SB203580 (p38 MAPK inhibitor), SP600125 (JNK inhibitor), LY294002 (PI3K inhibitor), and BAY11-7082 (NK-κB inhibitor), and they were obtained from Biomol Research Laboratories (Plymouth Meeting, PA, United States).

Techniques: Isolation, Expressing, Quantitative RT-PCR, Protein Concentration, Enzyme-linked Immunosorbent Assay, Mutagenesis, Concentration Assay, Western Blot, Mouse Assay

p38-MAPK and ERK pathways in DC polarization. (A, B) Control LPS-mDC (black bars) or DC pre-treated with 25 μM SB203580 (A) or with 40μM PD98059 (B) before addition of LPS at day 6 (grey bars) were cocultured with T cells. Data are shown for 1/20 DC/T cell ratio and were similar for other ratios. Secretions of IFNγ, IL-5 and IL-13 were measured in coculture supernatants at day 5. Cytokine secretion was normalized to 100% for control mDC. Mean ± SD of three independent experiments. (C, D) p38-MAPK inhibitor prevents Th2 polarization of LPS-stimulated DC. Control LPS-stimulated DC (black bars), LPS-stimulated DC pre-treated with 1-MT (opened bars) or LPS-stimulated DC pre-treated with SB203580 and 1-MT (hatched bars) were cultured with T cells. Secretions of IFNγ (C), IL-5 and IL-13 (D) were measured in coculture supernatants at day 5. Cytokine secretion was normalized to 100% for control mDC. Mean ± SD of three independent experiments. (E, F) MEK/ERK pathway inhibitor restores the Th1 polarization of DC treated by 1-MT and LPS. Control LPS-stimulated DC (black bars), LPS-stimulated DC pre-treated with 1-MT (opened bars) or LPS-stimulated DC pre-treated with PD98059 and 1-MT (grey bars) were cultured with T cells. Secretions of IFNγ (E), IL-5 and IL-13 (F) were measured in the supernatants at day 5 of coculture. Cytokine secretion was normalized to 100% for control LPS-stimulated DC. Mean ± SD of three independent experiments.

Journal: Journal of immunology (Baltimore, Md. : 1950)

Article Title: 1-Methyl-tryptophan can interfere with TLR signaling in dendritic cells independently of IDO activity

doi:

Figure Lengend Snippet: p38-MAPK and ERK pathways in DC polarization. (A, B) Control LPS-mDC (black bars) or DC pre-treated with 25 μM SB203580 (A) or with 40μM PD98059 (B) before addition of LPS at day 6 (grey bars) were cocultured with T cells. Data are shown for 1/20 DC/T cell ratio and were similar for other ratios. Secretions of IFNγ, IL-5 and IL-13 were measured in coculture supernatants at day 5. Cytokine secretion was normalized to 100% for control mDC. Mean ± SD of three independent experiments. (C, D) p38-MAPK inhibitor prevents Th2 polarization of LPS-stimulated DC. Control LPS-stimulated DC (black bars), LPS-stimulated DC pre-treated with 1-MT (opened bars) or LPS-stimulated DC pre-treated with SB203580 and 1-MT (hatched bars) were cultured with T cells. Secretions of IFNγ (C), IL-5 and IL-13 (D) were measured in coculture supernatants at day 5. Cytokine secretion was normalized to 100% for control mDC. Mean ± SD of three independent experiments. (E, F) MEK/ERK pathway inhibitor restores the Th1 polarization of DC treated by 1-MT and LPS. Control LPS-stimulated DC (black bars), LPS-stimulated DC pre-treated with 1-MT (opened bars) or LPS-stimulated DC pre-treated with PD98059 and 1-MT (grey bars) were cultured with T cells. Secretions of IFNγ (E), IL-5 and IL-13 (F) were measured in the supernatants at day 5 of coculture. Cytokine secretion was normalized to 100% for control LPS-stimulated DC. Mean ± SD of three independent experiments.

Article Snippet: Control mature DC (mDC) were obtained by adding TLR ligands at day 6 for 24 h. When indicated, 40 μM PD98059, an inhibitor of MEK1/2 (Biomol, Plymouth Meeting, PA, USA), or 25 μM SB203580, an inhibitor of p38-MAPK (Biomol), were added 30 min before 1-MT treatment.

Techniques: Cell Culture

Differential effect of 1-MT on p38-MAPK, ERK and c-Fos activation induced by different TLR ligands. (A, B) Time course of p38 and ERK phosphorylation induced by 1-MT pre-treatment and TLR stimulation. DC were treated at day 5 with 1-MT (△) and stimulated at day 6 with LPS, pIC, PGN or Pam for the indicated periods of time. Control TLR-stimulated DC (■) were not treated with 1-MT. Phosphorylated and total p38 (A) and phosphorylated and total ERK (B) were quantified in cell lysates by ELISA. Results are shown as phosphorylated/total protein ratio. Data from one representative experiment out of three. (C) Time course of c-Fos phosphorylation induced by 1-MT pre-treatment and TLR stimulation. DC were treated at day 5 with 1-MT (△) and stimulated at day 6 with LPS, pIC, PGN or Pam for the indicated periods of time. Control TLR-stimulated DC (■) were not treated with 1-MT. Phosphorylated c-Fos was quantified in cell lysates and normalized compared to the total protein content. Results are shown as phosphorylated c-Fos (RLU)/μg protein ratio. Data from one representative experiment out of three.

Journal: Journal of immunology (Baltimore, Md. : 1950)

Article Title: 1-Methyl-tryptophan can interfere with TLR signaling in dendritic cells independently of IDO activity

doi:

Figure Lengend Snippet: Differential effect of 1-MT on p38-MAPK, ERK and c-Fos activation induced by different TLR ligands. (A, B) Time course of p38 and ERK phosphorylation induced by 1-MT pre-treatment and TLR stimulation. DC were treated at day 5 with 1-MT (△) and stimulated at day 6 with LPS, pIC, PGN or Pam for the indicated periods of time. Control TLR-stimulated DC (■) were not treated with 1-MT. Phosphorylated and total p38 (A) and phosphorylated and total ERK (B) were quantified in cell lysates by ELISA. Results are shown as phosphorylated/total protein ratio. Data from one representative experiment out of three. (C) Time course of c-Fos phosphorylation induced by 1-MT pre-treatment and TLR stimulation. DC were treated at day 5 with 1-MT (△) and stimulated at day 6 with LPS, pIC, PGN or Pam for the indicated periods of time. Control TLR-stimulated DC (■) were not treated with 1-MT. Phosphorylated c-Fos was quantified in cell lysates and normalized compared to the total protein content. Results are shown as phosphorylated c-Fos (RLU)/μg protein ratio. Data from one representative experiment out of three.

Techniques: Activation Assay, Enzyme-linked Immunosorbent Assay

Structured Review

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