Structured Review

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
https://www.bioz.com/result/p38 mapk activation inhibitor/product/Biomol GmbH
Average 86 stars, based on 1 article reviews
Price from $9.99 to $1999.99
p38 mapk activation inhibitor - by Bioz Stars, 2021-04
86/100 stars

Images

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

Related Articles

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.

Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 86
    Biomol GmbH p38 mapk inhibitor
    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
    P38 Mapk 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
    https://www.bioz.com/result/p38 mapk inhibitor/product/Biomol GmbH
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    p38 mapk inhibitor - by Bioz Stars, 2021-04
    86/100 stars
      Buy from Supplier

    86
    Biomol GmbH p38 mapk inhibitors
    <t>p38</t> <t>MAPK</t> inhibitor and NF-κB inhibitor reduced microbial activation of TL1A expression
    P38 Mapk Inhibitors, 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
    https://www.bioz.com/result/p38 mapk inhibitors/product/Biomol GmbH
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    p38 mapk inhibitors - by Bioz Stars, 2021-04
    86/100 stars
      Buy from Supplier

    86
    Biomol GmbH sb203580
    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
    Sb203580, 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
    https://www.bioz.com/result/sb203580/product/Biomol GmbH
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    sb203580 - by Bioz Stars, 2021-04
    86/100 stars
      Buy from Supplier

    86
    Biomol GmbH p38 mapk
    <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.
    P38 Mapk, 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
    https://www.bioz.com/result/p38 mapk/product/Biomol GmbH
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    p38 mapk - by Bioz Stars, 2021-04
    86/100 stars
      Buy from Supplier

    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

    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: Activity Assay

    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

    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.

    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: Activation Assay, Enzyme-linked Immunosorbent Assay