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  • 95
    Thermo Fisher enzyme linked immunosorbent assay elisa
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    Sild-Met-Leu treatment decreases inflammatory marker in hepatocytes and macrophages. Mouse hepatocytes (AML cells) and macrophages (RAW 264.7 cells), grown individually or in coculture, were treated with sildenafil (1 nM), metformin (0.1 mM), and leucine (0.5 mM) as indicated for 24 hours after induction with free fatty acids (FFA) and/or LPS. Nontreated cells (control) were included for comparison. ((a) and (b)) Monocyte chemotactic protein- (MCP-) 1 secretion in media of AML cells and of hepatocyte-macrophage coculture. Data are presented as mean ± SEM ( n = 4 to 10). ((c) to (e)) Protein expression of phosphorylated and total NF- κ B and <t>TNF-alpha</t> in AML 12 hepatocytes and RAW 264.7 macrophages. Quantitative data are presented as mean ± SEM ( n = 4), and representative blots are shown. (f) Macrophage tumor necrosis factor- (TNF-) alpha secretion was measured in the media. Data are presented as mean ± SEM ( n = 5).
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    Sild-Met-Leu treatment decreases inflammatory marker in hepatocytes and macrophages. Mouse hepatocytes (AML cells) and macrophages (RAW 264.7 cells), grown individually or in coculture, were treated with sildenafil (1 nM), metformin (0.1 mM), and leucine (0.5 mM) as indicated for 24 hours after induction with free fatty acids (FFA) and/or LPS. Nontreated cells (control) were included for comparison. ((a) and (b)) Monocyte chemotactic protein- (MCP-) 1 secretion in media of AML cells and of hepatocyte-macrophage coculture. Data are presented as mean ± SEM ( n = 4 to 10). ((c) to (e)) Protein expression of phosphorylated and total NF- κ B and <t>TNF-alpha</t> in AML 12 hepatocytes and RAW 264.7 macrophages. Quantitative data are presented as mean ± SEM ( n = 4), and representative blots are shown. (f) Macrophage tumor necrosis factor- (TNF-) alpha secretion was measured in the media. Data are presented as mean ± SEM ( n = 5).
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    Sild-Met-Leu treatment decreases inflammatory marker in hepatocytes and macrophages. Mouse hepatocytes (AML cells) and macrophages (RAW 264.7 cells), grown individually or in coculture, were treated with sildenafil (1 nM), metformin (0.1 mM), and leucine (0.5 mM) as indicated for 24 hours after induction with free fatty acids (FFA) and/or LPS. Nontreated cells (control) were included for comparison. ((a) and (b)) Monocyte chemotactic protein- (MCP-) 1 secretion in media of AML cells and of hepatocyte-macrophage coculture. Data are presented as mean ± SEM ( n = 4 to 10). ((c) to (e)) Protein expression of phosphorylated and total NF- κ B and <t>TNF-alpha</t> in AML 12 hepatocytes and RAW 264.7 macrophages. Quantitative data are presented as mean ± SEM ( n = 4), and representative blots are shown. (f) Macrophage tumor necrosis factor- (TNF-) alpha secretion was measured in the media. Data are presented as mean ± SEM ( n = 5).
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    <t>TNF</t> release by macrophages stimulated with supernatants of S. aureus. S. aureus strains were cultured in DMEM and treated with the indicated concentrations of linezolid as described in the text. Secreted proteins present in the supernatant were collected, followed by incubation for 20 h at 37°C with mouse splenic macrophages or peritoneal macrophages. The TNF levels were measured by <t>ELISA.</t> Linezolid itself (1× MIC and 2× MIC) did not induce TNF (data not shown).
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    <t>TNF</t> release by macrophages stimulated with supernatants of S. aureus. S. aureus strains were cultured in DMEM and treated with the indicated concentrations of linezolid as described in the text. Secreted proteins present in the supernatant were collected, followed by incubation for 20 h at 37°C with mouse splenic macrophages or peritoneal macrophages. The TNF levels were measured by <t>ELISA.</t> Linezolid itself (1× MIC and 2× MIC) did not induce TNF (data not shown).
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    Agmatine downregulates Zymosan-induced TNF-α, IL-1 β , and IL-6 in lung and BALF. At 6 hr after ZYM or Saline injection, the cytokines levels in lung and BALF tissue were measured using commercially available enzyme-linked <t>immunosorbent</t> assay <t>(ELISA)</t> kits. * P
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    Production of tumour necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 in lungs of mice receiving α-galactosylceramide (α-GalCer) and lipopolysaccharide (LPS). LPS was injected into the mice sensitized with α-GalCer 12 h before. The concentration of cytokines in lung tissues, bronchoalveolar lavage fluid and sera was determined 6 h after LPS injection by enzyme-linked <t>immunosorbent</t> assay. The experimental data are shown as the mean of triplicates ± standard deviation from three independent experiments. * P
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    PLD1 modulates <t>TNF-α</t> expression and release via phosphorylation of MEK1/2 and ERK1/2. MEFs from Pld1 +/+ and Pld1 −/− mice were stimulated with 1 mg/ml LPS for indicated time points. ( A) TNF-α release into the supernatant of MEFs after LPS stimulation was measured by <t>ELISA.</t> ( B – E ) Phosphorylation of SAPK/JNK, p38 and ERK1/2 was detected by Western blot after stimulation of MEFs with LPS for 30 min. and quantified via adjusted density using ImageJ. Same samples for quantification of total protein expression were used but applied to different gels/membranes. Cropped blots are shown. ( F – H ) Phosphorylation of MEK1/2 and protein abundance of EGR-1 was detected after LPS stimulation of MEFs for 30 min. using Western blot analysis and quantified via adjusted density using ImageJ. B-tubulin serves as loading control for the detection of EGR-1. Cropped blots are shown. ( I ) Egr-1 expression in MEFs was analyzed by qRT-PCR 5 hrs. after LPS stimulation. ( J ) ΔEgr-1 expression (basal-stimulated) of Pld1 +/+ and Pld1 −/− MEFs. N = 5. ( K ) Egr-1 expression in the liver of PLD1 deficient and control mice was determined by qRT-PCR. N = 9. Bar graphs depict mean values ± s.e.m. *P
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    PLD1 modulates <t>TNF-α</t> expression and release via phosphorylation of MEK1/2 and ERK1/2. MEFs from Pld1 +/+ and Pld1 −/− mice were stimulated with 1 mg/ml LPS for indicated time points. ( A) TNF-α release into the supernatant of MEFs after LPS stimulation was measured by <t>ELISA.</t> ( B – E ) Phosphorylation of SAPK/JNK, p38 and ERK1/2 was detected by Western blot after stimulation of MEFs with LPS for 30 min. and quantified via adjusted density using ImageJ. Same samples for quantification of total protein expression were used but applied to different gels/membranes. Cropped blots are shown. ( F – H ) Phosphorylation of MEK1/2 and protein abundance of EGR-1 was detected after LPS stimulation of MEFs for 30 min. using Western blot analysis and quantified via adjusted density using ImageJ. B-tubulin serves as loading control for the detection of EGR-1. Cropped blots are shown. ( I ) Egr-1 expression in MEFs was analyzed by qRT-PCR 5 hrs. after LPS stimulation. ( J ) ΔEgr-1 expression (basal-stimulated) of Pld1 +/+ and Pld1 −/− MEFs. N = 5. ( K ) Egr-1 expression in the liver of PLD1 deficient and control mice was determined by qRT-PCR. N = 9. Bar graphs depict mean values ± s.e.m. *P
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    Image Search Results


    Sild-Met-Leu treatment decreases inflammatory marker in hepatocytes and macrophages. Mouse hepatocytes (AML cells) and macrophages (RAW 264.7 cells), grown individually or in coculture, were treated with sildenafil (1 nM), metformin (0.1 mM), and leucine (0.5 mM) as indicated for 24 hours after induction with free fatty acids (FFA) and/or LPS. Nontreated cells (control) were included for comparison. ((a) and (b)) Monocyte chemotactic protein- (MCP-) 1 secretion in media of AML cells and of hepatocyte-macrophage coculture. Data are presented as mean ± SEM ( n = 4 to 10). ((c) to (e)) Protein expression of phosphorylated and total NF- κ B and TNF-alpha in AML 12 hepatocytes and RAW 264.7 macrophages. Quantitative data are presented as mean ± SEM ( n = 4), and representative blots are shown. (f) Macrophage tumor necrosis factor- (TNF-) alpha secretion was measured in the media. Data are presented as mean ± SEM ( n = 5).

    Journal: International Journal of Hepatology

    Article Title: A Combination of Leucine, Metformin, and Sildenafil Treats Nonalcoholic Fatty Liver Disease and Steatohepatitis in Mice

    doi: 10.1155/2016/9185987

    Figure Lengend Snippet: Sild-Met-Leu treatment decreases inflammatory marker in hepatocytes and macrophages. Mouse hepatocytes (AML cells) and macrophages (RAW 264.7 cells), grown individually or in coculture, were treated with sildenafil (1 nM), metformin (0.1 mM), and leucine (0.5 mM) as indicated for 24 hours after induction with free fatty acids (FFA) and/or LPS. Nontreated cells (control) were included for comparison. ((a) and (b)) Monocyte chemotactic protein- (MCP-) 1 secretion in media of AML cells and of hepatocyte-macrophage coculture. Data are presented as mean ± SEM ( n = 4 to 10). ((c) to (e)) Protein expression of phosphorylated and total NF- κ B and TNF-alpha in AML 12 hepatocytes and RAW 264.7 macrophages. Quantitative data are presented as mean ± SEM ( n = 4), and representative blots are shown. (f) Macrophage tumor necrosis factor- (TNF-) alpha secretion was measured in the media. Data are presented as mean ± SEM ( n = 5).

    Article Snippet: Monocyte chemotactic protein- (MCP-) 1 and tumor necrosis factor- (TNF-) α secretion was measured with the MCP1 Mouse Elisa kit and TNF-alpha Mouse Elisa kit (Abcam, Cambridge, MA, USA), respectively, according to manufacturer's instructions.

    Techniques: Marker, Expressing

    TNF release by macrophages stimulated with supernatants of S. aureus. S. aureus strains were cultured in DMEM and treated with the indicated concentrations of linezolid as described in the text. Secreted proteins present in the supernatant were collected, followed by incubation for 20 h at 37°C with mouse splenic macrophages or peritoneal macrophages. The TNF levels were measured by ELISA. Linezolid itself (1× MIC and 2× MIC) did not induce TNF (data not shown).

    Journal: Antimicrobial Agents and Chemotherapy

    Article Title: Subinhibitory Concentrations of Linezolid Reduce Staphylococcus aureus Virulence Factor Expression

    doi: 10.1128/AAC.48.2.546-555.2004

    Figure Lengend Snippet: TNF release by macrophages stimulated with supernatants of S. aureus. S. aureus strains were cultured in DMEM and treated with the indicated concentrations of linezolid as described in the text. Secreted proteins present in the supernatant were collected, followed by incubation for 20 h at 37°C with mouse splenic macrophages or peritoneal macrophages. The TNF levels were measured by ELISA. Linezolid itself (1× MIC and 2× MIC) did not induce TNF (data not shown).

    Article Snippet: TNF in the supernatants was determined by using the Mouse TNF-α DuoSet ELISA (R & D Systems, Inc., Minneapolis, Minn.).

    Techniques: Cell Culture, Incubation, Enzyme-linked Immunosorbent Assay

    Agmatine downregulates Zymosan-induced TNF-α, IL-1 β , and IL-6 in lung and BALF. At 6 hr after ZYM or Saline injection, the cytokines levels in lung and BALF tissue were measured using commercially available enzyme-linked immunosorbent assay (ELISA) kits. * P

    Journal: BioMed Research International

    Article Title: Agmatine Protects against Zymosan-Induced Acute Lung Injury in Mice by Inhibiting NF-κB-Mediated Inflammatory Response

    doi: 10.1155/2014/583736

    Figure Lengend Snippet: Agmatine downregulates Zymosan-induced TNF-α, IL-1 β , and IL-6 in lung and BALF. At 6 hr after ZYM or Saline injection, the cytokines levels in lung and BALF tissue were measured using commercially available enzyme-linked immunosorbent assay (ELISA) kits. * P

    Article Snippet: Measurement of Cytokine Production At 6 hrs after ZYM or NS injection, the cytokines levels in BALF and lung tissue were measured using commercially available enzyme-linked immunosorbent assay (ELISA) kits (mouse TNF-α, IL-1β , and IL-6 ELISA kits are from Boster Biotechnology, Wuhan, China).

    Techniques: Injection, Enzyme-linked Immunosorbent Assay

    Production of tumour necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 in lungs of mice receiving α-galactosylceramide (α-GalCer) and lipopolysaccharide (LPS). LPS was injected into the mice sensitized with α-GalCer 12 h before. The concentration of cytokines in lung tissues, bronchoalveolar lavage fluid and sera was determined 6 h after LPS injection by enzyme-linked immunosorbent assay. The experimental data are shown as the mean of triplicates ± standard deviation from three independent experiments. * P

    Journal: Clinical and Experimental Immunology

    Article Title: The mechanism of development of acute lung injury in lethal endotoxic shock using ?-galactosylceramide sensitization

    doi: 10.1111/j.1365-2249.2008.03603.x

    Figure Lengend Snippet: Production of tumour necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 in lungs of mice receiving α-galactosylceramide (α-GalCer) and lipopolysaccharide (LPS). LPS was injected into the mice sensitized with α-GalCer 12 h before. The concentration of cytokines in lung tissues, bronchoalveolar lavage fluid and sera was determined 6 h after LPS injection by enzyme-linked immunosorbent assay. The experimental data are shown as the mean of triplicates ± standard deviation from three independent experiments. * P

    Article Snippet: The level of each cytokine was measured with enzyme-linked immunosorbent assay (ELISA) kits (TNF-α and IL-1β kits from R & D company; IL-6 from Biosciences).

    Techniques: Mouse Assay, Injection, Concentration Assay, Enzyme-linked Immunosorbent Assay, Standard Deviation

    Inhibition of caspase-9 enhanced pro-inflammatory mediator triggered necroptotic cell death in HepG2 cells. Elisa for human TNF-α was tested in HepG2 cells after treatment with z-IETD-FMK ( A ); chloroquine ( B ); and rapamycin (C) . TLR4 ( D ), TNF-α ( E ) mRNA, and NF-κB/p65 ( F ) protein levels were also evaluated after the knock down of TLR4 using siRNA. RIP1 and RIP3 protein levels ( G ) were measured using Western blotting. Beclin 1, LC3II and RIP1 protein expression levels were also evaluated after treating rapamycin (20 nM) ( H ) and necrostatin-1 (50 μM) ( I ), respectively. Data presented are expressed as Mean ± SD (n = 6) and experimental groups marked by different letters represent significant differences between groups at p

    Journal: Scientific Reports

    Article Title: Inhibition of caspase-9 aggravates acute liver injury through suppression of cytoprotective autophagy

    doi: 10.1038/srep32447

    Figure Lengend Snippet: Inhibition of caspase-9 enhanced pro-inflammatory mediator triggered necroptotic cell death in HepG2 cells. Elisa for human TNF-α was tested in HepG2 cells after treatment with z-IETD-FMK ( A ); chloroquine ( B ); and rapamycin (C) . TLR4 ( D ), TNF-α ( E ) mRNA, and NF-κB/p65 ( F ) protein levels were also evaluated after the knock down of TLR4 using siRNA. RIP1 and RIP3 protein levels ( G ) were measured using Western blotting. Beclin 1, LC3II and RIP1 protein expression levels were also evaluated after treating rapamycin (20 nM) ( H ) and necrostatin-1 (50 μM) ( I ), respectively. Data presented are expressed as Mean ± SD (n = 6) and experimental groups marked by different letters represent significant differences between groups at p

    Article Snippet: Enzyme-linked immunosorbent assay (ELISA) assay Human TNF-α and NF-κB were tested utilizing TNF-α and NF-κB Human Ultrasensitive ELISA Kits (Life technologies, CA, USA), and mouse TNF-α and IL-1β were examined using the ELISA Kits from R & D systems (Minnesota, USA).

    Techniques: Inhibition, Enzyme-linked Immunosorbent Assay, Western Blot, Expressing

    Caspase-9 inhibition remarkably elevated necroptotic markers induced by inflammation in mice. In mouse liver, TNF-α ( A ) and IL-1β ( B ) levels, as well as DNA-binding activity of NF-κB ( C ) were detected by ELISA. Protein levels were also measured by western blotting including total IκB-α protein expression in cytosol, RIP1 and RIP3 in mouse liver ( D ). Data presented are expressed as Mean ± SD (n = 6) and experimental groups marked by different letters represent significant differences between groups at p

    Journal: Scientific Reports

    Article Title: Inhibition of caspase-9 aggravates acute liver injury through suppression of cytoprotective autophagy

    doi: 10.1038/srep32447

    Figure Lengend Snippet: Caspase-9 inhibition remarkably elevated necroptotic markers induced by inflammation in mice. In mouse liver, TNF-α ( A ) and IL-1β ( B ) levels, as well as DNA-binding activity of NF-κB ( C ) were detected by ELISA. Protein levels were also measured by western blotting including total IκB-α protein expression in cytosol, RIP1 and RIP3 in mouse liver ( D ). Data presented are expressed as Mean ± SD (n = 6) and experimental groups marked by different letters represent significant differences between groups at p

    Article Snippet: Enzyme-linked immunosorbent assay (ELISA) assay Human TNF-α and NF-κB were tested utilizing TNF-α and NF-κB Human Ultrasensitive ELISA Kits (Life technologies, CA, USA), and mouse TNF-α and IL-1β were examined using the ELISA Kits from R & D systems (Minnesota, USA).

    Techniques: Inhibition, Mouse Assay, Binding Assay, Activity Assay, Enzyme-linked Immunosorbent Assay, Western Blot, Expressing

    Inhibition of caspase-9 further suppressed autophagy, decreased apoptosis and promoted inflammation-triggered necroptosis in AML12 cells. Protein expressions were also tested by Western blotting including Beclin 1, LC3II, RIP1, caspase-9 and cleaved PARP ( A ). TNF-α protein level was also evaluated using ELISA ( B ). Data presented are expressed as Mean ± SD (n = 6) and experimental groups marked by different letters represent significant differences between groups at p

    Journal: Scientific Reports

    Article Title: Inhibition of caspase-9 aggravates acute liver injury through suppression of cytoprotective autophagy

    doi: 10.1038/srep32447

    Figure Lengend Snippet: Inhibition of caspase-9 further suppressed autophagy, decreased apoptosis and promoted inflammation-triggered necroptosis in AML12 cells. Protein expressions were also tested by Western blotting including Beclin 1, LC3II, RIP1, caspase-9 and cleaved PARP ( A ). TNF-α protein level was also evaluated using ELISA ( B ). Data presented are expressed as Mean ± SD (n = 6) and experimental groups marked by different letters represent significant differences between groups at p

    Article Snippet: Enzyme-linked immunosorbent assay (ELISA) assay Human TNF-α and NF-κB were tested utilizing TNF-α and NF-κB Human Ultrasensitive ELISA Kits (Life technologies, CA, USA), and mouse TNF-α and IL-1β were examined using the ELISA Kits from R & D systems (Minnesota, USA).

    Techniques: Inhibition, Western Blot, Enzyme-linked Immunosorbent Assay

    PLD1 modulates TNF-α expression and release via phosphorylation of MEK1/2 and ERK1/2. MEFs from Pld1 +/+ and Pld1 −/− mice were stimulated with 1 mg/ml LPS for indicated time points. ( A) TNF-α release into the supernatant of MEFs after LPS stimulation was measured by ELISA. ( B – E ) Phosphorylation of SAPK/JNK, p38 and ERK1/2 was detected by Western blot after stimulation of MEFs with LPS for 30 min. and quantified via adjusted density using ImageJ. Same samples for quantification of total protein expression were used but applied to different gels/membranes. Cropped blots are shown. ( F – H ) Phosphorylation of MEK1/2 and protein abundance of EGR-1 was detected after LPS stimulation of MEFs for 30 min. using Western blot analysis and quantified via adjusted density using ImageJ. B-tubulin serves as loading control for the detection of EGR-1. Cropped blots are shown. ( I ) Egr-1 expression in MEFs was analyzed by qRT-PCR 5 hrs. after LPS stimulation. ( J ) ΔEgr-1 expression (basal-stimulated) of Pld1 +/+ and Pld1 −/− MEFs. N = 5. ( K ) Egr-1 expression in the liver of PLD1 deficient and control mice was determined by qRT-PCR. N = 9. Bar graphs depict mean values ± s.e.m. *P

    Journal: Scientific Reports

    Article Title: Phospholipase D1 regulation of TNF-alpha protects against responses to LPS

    doi: 10.1038/s41598-018-28331-y

    Figure Lengend Snippet: PLD1 modulates TNF-α expression and release via phosphorylation of MEK1/2 and ERK1/2. MEFs from Pld1 +/+ and Pld1 −/− mice were stimulated with 1 mg/ml LPS for indicated time points. ( A) TNF-α release into the supernatant of MEFs after LPS stimulation was measured by ELISA. ( B – E ) Phosphorylation of SAPK/JNK, p38 and ERK1/2 was detected by Western blot after stimulation of MEFs with LPS for 30 min. and quantified via adjusted density using ImageJ. Same samples for quantification of total protein expression were used but applied to different gels/membranes. Cropped blots are shown. ( F – H ) Phosphorylation of MEK1/2 and protein abundance of EGR-1 was detected after LPS stimulation of MEFs for 30 min. using Western blot analysis and quantified via adjusted density using ImageJ. B-tubulin serves as loading control for the detection of EGR-1. Cropped blots are shown. ( I ) Egr-1 expression in MEFs was analyzed by qRT-PCR 5 hrs. after LPS stimulation. ( J ) ΔEgr-1 expression (basal-stimulated) of Pld1 +/+ and Pld1 −/− MEFs. N = 5. ( K ) Egr-1 expression in the liver of PLD1 deficient and control mice was determined by qRT-PCR. N = 9. Bar graphs depict mean values ± s.e.m. *P

    Article Snippet: Enzyme-linked Immunosorbent Assay (ELISA) TNF-α and IL-6 levels in the supernatant of mouse embryonic fibroblasts (MEFs) and in plasma of septic mice were determined by specific ELISA (BD Pharmingen) following the manufacturer’s protocol.

    Techniques: Expressing, Mouse Assay, Enzyme-linked Immunosorbent Assay, Western Blot, Quantitative RT-PCR

    PLD1 deficiency decreases mortality in LPS-induced sepsis by modulating TNF-α expression and release. ( A ) Pld1 +/+ and Pld1 −/− mice were injected with 10 mg/kg bodyweight LPS and survival was monitored for 100 hrs. N = 10 per group. P-value = 0.0332, Log-rank Mantel-Cox test. ( B,C ) Pld1 +/+ and Pld1 −/− mice were injected with 4 mg/kg bodyweight LPS and serum TNF-α ( B ) and IL-6 ( C ) were measured at indicated time points after LPS injection and under basal conditions using ELISA. ( D ) TNF-α expression in liver tissue was analyzed by qRT-PCR at indicated time points following LPS injection. N = 5 ( B – D ). Bar graphs depict mean values ± s.e.m. *P

    Journal: Scientific Reports

    Article Title: Phospholipase D1 regulation of TNF-alpha protects against responses to LPS

    doi: 10.1038/s41598-018-28331-y

    Figure Lengend Snippet: PLD1 deficiency decreases mortality in LPS-induced sepsis by modulating TNF-α expression and release. ( A ) Pld1 +/+ and Pld1 −/− mice were injected with 10 mg/kg bodyweight LPS and survival was monitored for 100 hrs. N = 10 per group. P-value = 0.0332, Log-rank Mantel-Cox test. ( B,C ) Pld1 +/+ and Pld1 −/− mice were injected with 4 mg/kg bodyweight LPS and serum TNF-α ( B ) and IL-6 ( C ) were measured at indicated time points after LPS injection and under basal conditions using ELISA. ( D ) TNF-α expression in liver tissue was analyzed by qRT-PCR at indicated time points following LPS injection. N = 5 ( B – D ). Bar graphs depict mean values ± s.e.m. *P

    Article Snippet: Enzyme-linked Immunosorbent Assay (ELISA) TNF-α and IL-6 levels in the supernatant of mouse embryonic fibroblasts (MEFs) and in plasma of septic mice were determined by specific ELISA (BD Pharmingen) following the manufacturer’s protocol.

    Techniques: Expressing, Mouse Assay, Injection, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR

    Inhibitory effect of MELT on the production of nitrite and proinflammatory cytokine, TNF-α induced by LPS treatment in RAW264.7 cells. RAW264.7 cells were treated with MELT for 30 min followed by LPS (100 ng/ml) treatment. The content of nitrite was measured by Griess assay, TNF-α by ELISA assay. * P

    Journal: Pharmacognosy Magazine

    Article Title: Hepatoprotective effects of Limonium tetragonum, edible medicinal halophyte growing near seashores

    doi: 10.4103/0973-1296.139783

    Figure Lengend Snippet: Inhibitory effect of MELT on the production of nitrite and proinflammatory cytokine, TNF-α induced by LPS treatment in RAW264.7 cells. RAW264.7 cells were treated with MELT for 30 min followed by LPS (100 ng/ml) treatment. The content of nitrite was measured by Griess assay, TNF-α by ELISA assay. * P

    Article Snippet: The concentration of TNF-a in the culture medium was determined by a mouse TNF enzyme-linked immunosorbent assay (ELISA) kit (BD Biosciences, San Jose, CA, USA).

    Techniques: Griess Assay, Enzyme-linked Immunosorbent Assay