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anti intercellular adhesion molecule 1  (Proteintech)


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    Structured Review

    Proteintech anti intercellular adhesion molecule 1
    Anti Intercellular Adhesion Molecule 1, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 400 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+intercellular+adhesion+molecule+1/Icam-1+Antibody/pmc12719248-72-39-44
    Average 96 stars, based on 400 article reviews
    anti intercellular adhesion molecule 1 - by Bioz Stars, 2026-09
    96/100 stars

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    Related Articles

    Blocking Assay:

    Article Title: Precise Investigation of the Efficacy of Multicomponent Drugs Against Pneumonia Infected With Influenza Virus
    Article Snippet: Thirty micrograms of each sample was loaded on 10% SDS-PAGE gels, and protein blots were transferred onto polyvinylidene fluoride membranes (Millipore, United States ). .. After blocking with 5% nonfat milk, the blots were incubated overnight at 4°C with the following primary antibodies: anti-glyceraldehyde-3-phosphate dehydrogenase (GAPDH, Proteintech, 10494-1-AP), anti-intercellular adhesion molecule-1 (ICAM-1, Proteintech, 16174-1-AP) and anti-transferrin (Proteintech, 17435-1-AP). ..

    Incubation:

    Article Title: Precise Investigation of the Efficacy of Multicomponent Drugs Against Pneumonia Infected With Influenza Virus
    Article Snippet: Thirty micrograms of each sample was loaded on 10% SDS-PAGE gels, and protein blots were transferred onto polyvinylidene fluoride membranes (Millipore, United States ). .. After blocking with 5% nonfat milk, the blots were incubated overnight at 4°C with the following primary antibodies: anti-glyceraldehyde-3-phosphate dehydrogenase (GAPDH, Proteintech, 10494-1-AP), anti-intercellular adhesion molecule-1 (ICAM-1, Proteintech, 16174-1-AP) and anti-transferrin (Proteintech, 17435-1-AP). ..

    Article Title: CD58 reshapes the immunosuppressive microenvironment in gliomas through PD-L1 upregulation
    Article Snippet: Protein lysates were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and transferred onto polyvinylidene fluoride (PVDF) membranes (Millipore, Billerica, MA, USA). .. Membranes were blocked with 5% non-fat milk in Tris-buffered saline containing 0.1% Tween-20 (TBST) for 1 hour at room temperature, followed by overnight incubation at 4°C with the following primary antibodies diluted in TBST: anti-CD58 (1:500, Proteintech, Wuhan, China), anti-intercellular adhesion molecule-1 (ICAM-1, 1:1000, Proteintech), anti-PD-L1 (1:2000, Proteintech), anti-vimentin (1:2000, Proteintech), and anti-glyceraldehyde-3-phosphate dehydrogenase (GAPDH, 1:3000, Proteintech). .. After three washes with TBST, membranes were incubated with horseradish peroxidase (HRP)-conjugated secondary antibodies (1:3000, Zhongshan Golden Bridge Biotechnology, Beijing, China) for 2 hour at room temperature.

    other:

    Article Title: Casticin prevents DSS induced ulcerative colitis in mice through inhibitions of NF-κB pathway and ROS signaling.
    Article Snippet: Department of Pharmacology of Chinese Medicine, School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, China Department of Spine Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China Correspondence Linzhong Yu, Department of Pharmacology of Chinese Medicine, Southern Medical University; No.1023, Shatainan Road, Guangzhou, Guangdong Province 510515, China.. Email: yulzh@fimmu.com

    Saline:

    Article Title: CD58 reshapes the immunosuppressive microenvironment in gliomas through PD-L1 upregulation
    Article Snippet: Protein lysates were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and transferred onto polyvinylidene fluoride (PVDF) membranes (Millipore, Billerica, MA, USA). .. Membranes were blocked with 5% non-fat milk in Tris-buffered saline containing 0.1% Tween-20 (TBST) for 1 hour at room temperature, followed by overnight incubation at 4°C with the following primary antibodies diluted in TBST: anti-CD58 (1:500, Proteintech, Wuhan, China), anti-intercellular adhesion molecule-1 (ICAM-1, 1:1000, Proteintech), anti-PD-L1 (1:2000, Proteintech), anti-vimentin (1:2000, Proteintech), and anti-glyceraldehyde-3-phosphate dehydrogenase (GAPDH, 1:3000, Proteintech). .. After three washes with TBST, membranes were incubated with horseradish peroxidase (HRP)-conjugated secondary antibodies (1:3000, Zhongshan Golden Bridge Biotechnology, Beijing, China) for 2 hour at room temperature.

    Recombinant:

    Article Title: SARS-CoV-2 ORF7a activates endothelium to release von Willebrand factor that promotes thrombosis
    Article Snippet: .. Primary antibodies used were β-actin antibody (Biotechne, Minneapolis, MN), recombinant anti-SARS-CoV2 Orf7a antibody (Abcam, Cambridge, UK), anti-intercellular adhesion molecule 1 (Proteintech, Rosemont, IL), and anti-αtubulin monoclonal antibody (Proteintech, Rosemont, IL), as well as rabbit anti-VWF (Agilent Diagnostics, Santa Clara, CA). .. The membrane was then washed three times with TBST and incubated for one hour with horseradish peroxidase (HRP)-conjugated secondary antibodies (Abcam, Cambridge, UK or LI-COR Biosciences, Lincoln, NE or Cell Signaling Technology, Danvers, MA), diluted 1:5,000 in blocking buffer.



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    Expression levels of hyaluronidase (Hyal)-1 (A) , CD44 (B) and receptor for hyaluronan-mediated motility (RHAMM) (C) in the retinal lysates of non-diabetic control rats (C) (n=12) and diabetic rats (D) (n=12) were determined by Western blot analysis. After determination of the intensity of the protein bands, intensities were adjusted to those of β-actin in the samples. Oxidative stress was monitored with the use of 2’,7’-Dichlorofluorescein (DCF) fluorescence intensity analysis (D) . Results are expressed as mean ± standard deviation. Ultra-Low molecular weight hyaluronan (ULMW-HA) induces breakdown of blood-retinal barrier (E) . ULMW-HA was injected intravitreally at the dose of 50 ng in 5 µL in one eye and the same volume of phosphate-buffered saline (PBS) was injected in the contralateral eye of normal rats. The BRB was quantified with the fluorescein isothiocyanate-conjugated dextran technique. Results are expressed as mean ± standard deviation of 12 rats. *p < 0.05 compared to the values obtained from PBS-injected eyes. (independent t-test). Western blot analysis of retinas demonstrated that intravitreal injection of ULMW-HA induced significant upregulation of the expression of phospho-NF-κB (F) , phospho-ERK1/2 (G) , vascular endothelial growth factor (VEGF) (H) , intercellular <t>adhesion</t> <t>molecule-1</t> (ICAM-1) (I) , vascular cell adhesion molecule-1 (VCAM-1) (J) and high-mobility group box-1 (HMGB1) (K) . Results are expressed as mean ± standard deviation or standard error of mean of 8–10 rats in each group (*p < 0.05; independent t-test).
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    Expression levels of hyaluronidase (Hyal)-1 (A) , CD44 (B) and receptor for hyaluronan-mediated motility (RHAMM) (C) in the retinal lysates of non-diabetic control rats (C) (n=12) and diabetic rats (D) (n=12) were determined by Western blot analysis. After determination of the intensity of the protein bands, intensities were adjusted to those of β-actin in the samples. Oxidative stress was monitored with the use of 2’,7’-Dichlorofluorescein (DCF) fluorescence intensity analysis (D) . Results are expressed as mean ± standard deviation. Ultra-Low molecular weight hyaluronan (ULMW-HA) induces breakdown of blood-retinal barrier (E) . ULMW-HA was injected intravitreally at the dose of 50 ng in 5 µL in one eye and the same volume of phosphate-buffered saline (PBS) was injected in the contralateral eye of normal rats. The BRB was quantified with the fluorescein isothiocyanate-conjugated dextran technique. Results are expressed as mean ± standard deviation of 12 rats. *p < 0.05 compared to the values obtained from PBS-injected eyes. (independent t-test). Western blot analysis of retinas demonstrated that intravitreal injection of ULMW-HA induced significant upregulation of the expression of phospho-NF-κB (F) , phospho-ERK1/2 (G) , vascular endothelial growth factor (VEGF) (H) , intercellular <t>adhesion</t> <t>molecule-1</t> (ICAM-1) (I) , vascular cell adhesion molecule-1 (VCAM-1) (J) and high-mobility group box-1 (HMGB1) (K) . Results are expressed as mean ± standard deviation or standard error of mean of 8–10 rats in each group (*p < 0.05; independent t-test).
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    Proteintech anti intercellular adhesion molecule 1
    Expression levels of hyaluronidase (Hyal)-1 (A) , CD44 (B) and receptor for hyaluronan-mediated motility (RHAMM) (C) in the retinal lysates of non-diabetic control rats (C) (n=12) and diabetic rats (D) (n=12) were determined by Western blot analysis. After determination of the intensity of the protein bands, intensities were adjusted to those of β-actin in the samples. Oxidative stress was monitored with the use of 2’,7’-Dichlorofluorescein (DCF) fluorescence intensity analysis (D) . Results are expressed as mean ± standard deviation. Ultra-Low molecular weight hyaluronan (ULMW-HA) induces breakdown of blood-retinal barrier (E) . ULMW-HA was injected intravitreally at the dose of 50 ng in 5 µL in one eye and the same volume of phosphate-buffered saline (PBS) was injected in the contralateral eye of normal rats. The BRB was quantified with the fluorescein isothiocyanate-conjugated dextran technique. Results are expressed as mean ± standard deviation of 12 rats. *p < 0.05 compared to the values obtained from PBS-injected eyes. (independent t-test). Western blot analysis of retinas demonstrated that intravitreal injection of ULMW-HA induced significant upregulation of the expression of phospho-NF-κB (F) , phospho-ERK1/2 (G) , vascular endothelial growth factor (VEGF) (H) , intercellular <t>adhesion</t> <t>molecule-1</t> (ICAM-1) (I) , vascular cell adhesion molecule-1 (VCAM-1) (J) and high-mobility group box-1 (HMGB1) (K) . Results are expressed as mean ± standard deviation or standard error of mean of 8–10 rats in each group (*p < 0.05; independent t-test).
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    Santa Cruz Biotechnology intercellular adhesion molecule 1
    Expression levels of hyaluronidase (Hyal)-1 (A) , CD44 (B) and receptor for hyaluronan-mediated motility (RHAMM) (C) in the retinal lysates of non-diabetic control rats (C) (n=12) and diabetic rats (D) (n=12) were determined by Western blot analysis. After determination of the intensity of the protein bands, intensities were adjusted to those of β-actin in the samples. Oxidative stress was monitored with the use of 2’,7’-Dichlorofluorescein (DCF) fluorescence intensity analysis (D) . Results are expressed as mean ± standard deviation. Ultra-Low molecular weight hyaluronan (ULMW-HA) induces breakdown of blood-retinal barrier (E) . ULMW-HA was injected intravitreally at the dose of 50 ng in 5 µL in one eye and the same volume of phosphate-buffered saline (PBS) was injected in the contralateral eye of normal rats. The BRB was quantified with the fluorescein isothiocyanate-conjugated dextran technique. Results are expressed as mean ± standard deviation of 12 rats. *p < 0.05 compared to the values obtained from PBS-injected eyes. (independent t-test). Western blot analysis of retinas demonstrated that intravitreal injection of ULMW-HA induced significant upregulation of the expression of phospho-NF-κB (F) , phospho-ERK1/2 (G) , vascular endothelial growth factor (VEGF) (H) , intercellular <t>adhesion</t> <t>molecule-1</t> (ICAM-1) (I) , vascular cell adhesion molecule-1 (VCAM-1) (J) and high-mobility group box-1 (HMGB1) (K) . Results are expressed as mean ± standard deviation or standard error of mean of 8–10 rats in each group (*p < 0.05; independent t-test).
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    Expression levels of hyaluronidase (Hyal)-1 (A) , CD44 (B) and receptor for hyaluronan-mediated motility (RHAMM) (C) in the retinal lysates of non-diabetic control rats (C) (n=12) and diabetic rats (D) (n=12) were determined by Western blot analysis. After determination of the intensity of the protein bands, intensities were adjusted to those of β-actin in the samples. Oxidative stress was monitored with the use of 2’,7’-Dichlorofluorescein (DCF) fluorescence intensity analysis (D) . Results are expressed as mean ± standard deviation. Ultra-Low molecular weight hyaluronan (ULMW-HA) induces breakdown of blood-retinal barrier (E) . ULMW-HA was injected intravitreally at the dose of 50 ng in 5 µL in one eye and the same volume of phosphate-buffered saline (PBS) was injected in the contralateral eye of normal rats. The BRB was quantified with the fluorescein isothiocyanate-conjugated dextran technique. Results are expressed as mean ± standard deviation of 12 rats. *p < 0.05 compared to the values obtained from PBS-injected eyes. (independent t-test). Western blot analysis of retinas demonstrated that intravitreal injection of ULMW-HA induced significant upregulation of the expression of phospho-NF-κB (F) , phospho-ERK1/2 (G) , vascular endothelial growth factor (VEGF) (H) , intercellular <t>adhesion</t> <t>molecule-1</t> (ICAM-1) (I) , vascular cell adhesion molecule-1 (VCAM-1) (J) and high-mobility group box-1 (HMGB1) (K) . Results are expressed as mean ± standard deviation or standard error of mean of 8–10 rats in each group (*p < 0.05; independent t-test).
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    Expression levels of hyaluronidase (Hyal)-1 (A) , CD44 (B) and receptor for hyaluronan-mediated motility (RHAMM) (C) in the retinal lysates of non-diabetic control rats (C) (n=12) and diabetic rats (D) (n=12) were determined by Western blot analysis. After determination of the intensity of the protein bands, intensities were adjusted to those of β-actin in the samples. Oxidative stress was monitored with the use of 2’,7’-Dichlorofluorescein (DCF) fluorescence intensity analysis (D) . Results are expressed as mean ± standard deviation. Ultra-Low molecular weight hyaluronan (ULMW-HA) induces breakdown of blood-retinal barrier (E) . ULMW-HA was injected intravitreally at the dose of 50 ng in 5 µL in one eye and the same volume of phosphate-buffered saline (PBS) was injected in the contralateral eye of normal rats. The BRB was quantified with the fluorescein isothiocyanate-conjugated dextran technique. Results are expressed as mean ± standard deviation of 12 rats. *p < 0.05 compared to the values obtained from PBS-injected eyes. (independent t-test). Western blot analysis of retinas demonstrated that intravitreal injection of ULMW-HA induced significant upregulation of the expression of phospho-NF-κB (F) , phospho-ERK1/2 (G) , vascular endothelial growth factor (VEGF) (H) , intercellular <t>adhesion</t> <t>molecule-1</t> (ICAM-1) (I) , vascular cell adhesion molecule-1 (VCAM-1) (J) and high-mobility group box-1 (HMGB1) (K) . Results are expressed as mean ± standard deviation or standard error of mean of 8–10 rats in each group (*p < 0.05; independent t-test).
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    Santa Cruz Biotechnology antibodies against intercellular adhesion molecule 1
    Expression levels of hyaluronidase (Hyal)-1 (A) , CD44 (B) and receptor for hyaluronan-mediated motility (RHAMM) (C) in the retinal lysates of non-diabetic control rats (C) (n=12) and diabetic rats (D) (n=12) were determined by Western blot analysis. After determination of the intensity of the protein bands, intensities were adjusted to those of β-actin in the samples. Oxidative stress was monitored with the use of 2’,7’-Dichlorofluorescein (DCF) fluorescence intensity analysis (D) . Results are expressed as mean ± standard deviation. Ultra-Low molecular weight hyaluronan (ULMW-HA) induces breakdown of blood-retinal barrier (E) . ULMW-HA was injected intravitreally at the dose of 50 ng in 5 µL in one eye and the same volume of phosphate-buffered saline (PBS) was injected in the contralateral eye of normal rats. The BRB was quantified with the fluorescein isothiocyanate-conjugated dextran technique. Results are expressed as mean ± standard deviation of 12 rats. *p < 0.05 compared to the values obtained from PBS-injected eyes. (independent t-test). Western blot analysis of retinas demonstrated that intravitreal injection of ULMW-HA induced significant upregulation of the expression of phospho-NF-κB (F) , phospho-ERK1/2 (G) , vascular endothelial growth factor (VEGF) (H) , intercellular <t>adhesion</t> <t>molecule-1</t> (ICAM-1) (I) , vascular cell adhesion molecule-1 (VCAM-1) (J) and high-mobility group box-1 (HMGB1) (K) . Results are expressed as mean ± standard deviation or standard error of mean of 8–10 rats in each group (*p < 0.05; independent t-test).
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    Santa Cruz Biotechnology antibodies against intercellular adhesion molecule
    Compounds 3 – 6 suppress TNF-α/IFN-γ-induced <t>ICAM-1</t> expression ( A , B ) and NF-κB Activation ( C ). The cells were pre-treated with compound 3 for 3 h and then stimulated with TNF-α/IFN-γ for 24 h. The expression of ICAM-1 was measured using Western blot. The p65 binding activity was detected by the p65 ELISA kit. The data are represented as the mean ± SD ( n = 3 independent experiments). ### p < 0.001 vs. untreated control group (gray column). * p < 0.05, ** p < 0.01, *** p < 0.001 vs. TNF-α/IFN-γ-treated group (red column).
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    Image Search Results


    Expression levels of hyaluronidase (Hyal)-1 (A) , CD44 (B) and receptor for hyaluronan-mediated motility (RHAMM) (C) in the retinal lysates of non-diabetic control rats (C) (n=12) and diabetic rats (D) (n=12) were determined by Western blot analysis. After determination of the intensity of the protein bands, intensities were adjusted to those of β-actin in the samples. Oxidative stress was monitored with the use of 2’,7’-Dichlorofluorescein (DCF) fluorescence intensity analysis (D) . Results are expressed as mean ± standard deviation. Ultra-Low molecular weight hyaluronan (ULMW-HA) induces breakdown of blood-retinal barrier (E) . ULMW-HA was injected intravitreally at the dose of 50 ng in 5 µL in one eye and the same volume of phosphate-buffered saline (PBS) was injected in the contralateral eye of normal rats. The BRB was quantified with the fluorescein isothiocyanate-conjugated dextran technique. Results are expressed as mean ± standard deviation of 12 rats. *p < 0.05 compared to the values obtained from PBS-injected eyes. (independent t-test). Western blot analysis of retinas demonstrated that intravitreal injection of ULMW-HA induced significant upregulation of the expression of phospho-NF-κB (F) , phospho-ERK1/2 (G) , vascular endothelial growth factor (VEGF) (H) , intercellular adhesion molecule-1 (ICAM-1) (I) , vascular cell adhesion molecule-1 (VCAM-1) (J) and high-mobility group box-1 (HMGB1) (K) . Results are expressed as mean ± standard deviation or standard error of mean of 8–10 rats in each group (*p < 0.05; independent t-test).

    Journal: Frontiers in Immunology

    Article Title: Dysregulated hyaluronan metabolism drives inflammation and angiogenesis in proliferative diabetic retinopathy

    doi: 10.3389/fimmu.2026.1724199

    Figure Lengend Snippet: Expression levels of hyaluronidase (Hyal)-1 (A) , CD44 (B) and receptor for hyaluronan-mediated motility (RHAMM) (C) in the retinal lysates of non-diabetic control rats (C) (n=12) and diabetic rats (D) (n=12) were determined by Western blot analysis. After determination of the intensity of the protein bands, intensities were adjusted to those of β-actin in the samples. Oxidative stress was monitored with the use of 2’,7’-Dichlorofluorescein (DCF) fluorescence intensity analysis (D) . Results are expressed as mean ± standard deviation. Ultra-Low molecular weight hyaluronan (ULMW-HA) induces breakdown of blood-retinal barrier (E) . ULMW-HA was injected intravitreally at the dose of 50 ng in 5 µL in one eye and the same volume of phosphate-buffered saline (PBS) was injected in the contralateral eye of normal rats. The BRB was quantified with the fluorescein isothiocyanate-conjugated dextran technique. Results are expressed as mean ± standard deviation of 12 rats. *p < 0.05 compared to the values obtained from PBS-injected eyes. (independent t-test). Western blot analysis of retinas demonstrated that intravitreal injection of ULMW-HA induced significant upregulation of the expression of phospho-NF-κB (F) , phospho-ERK1/2 (G) , vascular endothelial growth factor (VEGF) (H) , intercellular adhesion molecule-1 (ICAM-1) (I) , vascular cell adhesion molecule-1 (VCAM-1) (J) and high-mobility group box-1 (HMGB1) (K) . Results are expressed as mean ± standard deviation or standard error of mean of 8–10 rats in each group (*p < 0.05; independent t-test).

    Article Snippet: To determine the presence of Hyal-1, Hyal-2, HAS2, CD44, syndecan-1, heparan sulphate and RHAMM in the vitreous samples, equal volumes (10 μL) of vitreous samples were boiled in Laemmli’s sample buffer (1:1, v/v) under reducing condition for 10 min. Immunodetection was performed with the use of rabbit polyclonal anti-Hyal-1 antibody (1:1000, NBP2-16906, Novus Biologicals), mouse polyclonal anti-Hyal-2 antibody (1:1000, H00008692-B02P, Novus Biologicals), mouse monoclonal anti-HAS2 antibody (1:1000, ab140671, Abcam), rabbit monoclonal anti-CD44 antibody (1:1000, ab189524, Abcam), rabbit monoclonal anti-RHAMM antibody (1:1000, ab124729, Abcam), rabbit monoclonal anti-phospho-extracellular signal-regulated kinase (ERK)1/2 antibody (1:1000, MAB1018, R&D Systems), rabbit polyclonal anti-p65 subunit of nuclear factor-kappa B (phospho-NF-κB) (1:1000, NB100-82086, Novus Biologicals), rabbit polyclonal anti-high-mobility group box1 (HMGB1) (1:1000, Cat. no. ab18256, Abcam), mouse monoclonal anti-VEGF antibody (1:750, MAB293, R&D Systems), mouse monoclonal anti-intercellular adhesion molecule-1 (ICAM-1) antibody (1:100, sc-8439, Santa Cruz Biotechnology Inc.), and mouse monoclonal anti-vascular cell adhesion molecule-1 (VCAM-1) antibody (1:100, sc-13160, Santa Cruz Biotechnology Inc.).

    Techniques: Expressing, Control, Western Blot, Fluorescence, Standard Deviation, Molecular Weight, Injection, Saline

    Human retinal microvascular endothelial cells (HRMECs) were left untreated or stimulated with tumor necrosis factor-α (TNF-α) (5 ng/mL) for 24 h with or without apigenin (10 µg/mL). Protein expression of intercellular adhesion molecule-1 (ICAM-1) (A) and vascular cell adhesion molecule-1 (VCAM-1) (B) was determined by Western blot analysis. Adhesion of fluorescently labeled THP-1 monocytic cells to HRMECs monolayer was quantified (C) . Results are expressed as mean ± standard deviation or standard error of mean from three different experiments each performed in triplicate. One-way ANOVA and independent t-test were used for comparisons between three groups and two groups, respectively. *p < 0.05 compared with values obtained from untreated cells. #p < 0.05 compared with values obtained from cells treated with TNF-α (RFU = relative fluorescence unit).

    Journal: Frontiers in Immunology

    Article Title: Dysregulated hyaluronan metabolism drives inflammation and angiogenesis in proliferative diabetic retinopathy

    doi: 10.3389/fimmu.2026.1724199

    Figure Lengend Snippet: Human retinal microvascular endothelial cells (HRMECs) were left untreated or stimulated with tumor necrosis factor-α (TNF-α) (5 ng/mL) for 24 h with or without apigenin (10 µg/mL). Protein expression of intercellular adhesion molecule-1 (ICAM-1) (A) and vascular cell adhesion molecule-1 (VCAM-1) (B) was determined by Western blot analysis. Adhesion of fluorescently labeled THP-1 monocytic cells to HRMECs monolayer was quantified (C) . Results are expressed as mean ± standard deviation or standard error of mean from three different experiments each performed in triplicate. One-way ANOVA and independent t-test were used for comparisons between three groups and two groups, respectively. *p < 0.05 compared with values obtained from untreated cells. #p < 0.05 compared with values obtained from cells treated with TNF-α (RFU = relative fluorescence unit).

    Article Snippet: To determine the presence of Hyal-1, Hyal-2, HAS2, CD44, syndecan-1, heparan sulphate and RHAMM in the vitreous samples, equal volumes (10 μL) of vitreous samples were boiled in Laemmli’s sample buffer (1:1, v/v) under reducing condition for 10 min. Immunodetection was performed with the use of rabbit polyclonal anti-Hyal-1 antibody (1:1000, NBP2-16906, Novus Biologicals), mouse polyclonal anti-Hyal-2 antibody (1:1000, H00008692-B02P, Novus Biologicals), mouse monoclonal anti-HAS2 antibody (1:1000, ab140671, Abcam), rabbit monoclonal anti-CD44 antibody (1:1000, ab189524, Abcam), rabbit monoclonal anti-RHAMM antibody (1:1000, ab124729, Abcam), rabbit monoclonal anti-phospho-extracellular signal-regulated kinase (ERK)1/2 antibody (1:1000, MAB1018, R&D Systems), rabbit polyclonal anti-p65 subunit of nuclear factor-kappa B (phospho-NF-κB) (1:1000, NB100-82086, Novus Biologicals), rabbit polyclonal anti-high-mobility group box1 (HMGB1) (1:1000, Cat. no. ab18256, Abcam), mouse monoclonal anti-VEGF antibody (1:750, MAB293, R&D Systems), mouse monoclonal anti-intercellular adhesion molecule-1 (ICAM-1) antibody (1:100, sc-8439, Santa Cruz Biotechnology Inc.), and mouse monoclonal anti-vascular cell adhesion molecule-1 (VCAM-1) antibody (1:100, sc-13160, Santa Cruz Biotechnology Inc.).

    Techniques: Expressing, Western Blot, Labeling, Standard Deviation, Fluorescence

    Compounds 3 – 6 suppress TNF-α/IFN-γ-induced ICAM-1 expression ( A , B ) and NF-κB Activation ( C ). The cells were pre-treated with compound 3 for 3 h and then stimulated with TNF-α/IFN-γ for 24 h. The expression of ICAM-1 was measured using Western blot. The p65 binding activity was detected by the p65 ELISA kit. The data are represented as the mean ± SD ( n = 3 independent experiments). ### p < 0.001 vs. untreated control group (gray column). * p < 0.05, ** p < 0.01, *** p < 0.001 vs. TNF-α/IFN-γ-treated group (red column).

    Journal: International Journal of Molecular Sciences

    Article Title: Anti-Inflammatory Activity of Compounds Isolated from Digitalis purpurea L. in TNF-α/IFN-γ-Induced HaCaT Keratinocytes and a Three-Dimensionally Reconstructed Human Skin Model

    doi: 10.3390/ijms26167747

    Figure Lengend Snippet: Compounds 3 – 6 suppress TNF-α/IFN-γ-induced ICAM-1 expression ( A , B ) and NF-κB Activation ( C ). The cells were pre-treated with compound 3 for 3 h and then stimulated with TNF-α/IFN-γ for 24 h. The expression of ICAM-1 was measured using Western blot. The p65 binding activity was detected by the p65 ELISA kit. The data are represented as the mean ± SD ( n = 3 independent experiments). ### p < 0.001 vs. untreated control group (gray column). * p < 0.05, ** p < 0.01, *** p < 0.001 vs. TNF-α/IFN-γ-treated group (red column).

    Article Snippet: Antibodies against intercellular adhesion molecule (ICAM-1), Involucrin, COX-2, Loricrin, p-IκBα, IκBα, p65, p-JAK2, p-STAT1, p-STAT3, p-ERK, ERK, p-JNK, JNK, actin, PCNA, HRP-conjugated anti-mouse, and anti-rabbit IgG were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA) and Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Expressing, Activation Assay, Western Blot, Binding Assay, Activity Assay, Enzyme-linked Immunosorbent Assay, Control