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    MedChemExpress hacat cells
    <t>Aurantiamide</t> acetate suppresses dermal inflammation and restores skin barrier function through targeting JAK1. (A) Diagram of the molecular docking between aurantiamide acetate, an active ingredient in PO, and JAK1 (PDB: 6BBU). (B) Inhibitory effects of aurantiamide acetate on JAK1 tyrosine kinase activity detected by the ADP-Glo™ reagent. (C) siRNA-JAK1 silencing efficiency 24 h after transfection. (D) Relative mRNA expression levels of IL17A, IL4, IL1β and FLG were detected via quantitative PCR in <t>HaCaT</t> cells transfected with NC or JAK1 siRNA. (E) Aurantiamide acetate inhibits proinflammatory gene transcription in non-siRNA-treated HaCaT keratinocytes stimulated with TNF-α/IFN-γ. (F) Aurantiamide acetate upregulates skin barrier protective gene transcription in non-siRNA-targeted HaCaT keratinocytes stimulated with TNF-α/IFN-γ. (C–F) Cells were pretreated with aurantiamide acetate (25, 50, or 100 μM) or vehicle (0.1% DMSO) for 1 h before TNF-α (10 ng/mL) and IFN-γ (10 ng/mL) challenge for 18 h. Relative mRNA expression levels of IL6 , IL1β , PTGS2 (COX-2) , CCL17 (TARC) , IL8 , IL4 , IL17A , FLG , LORICRIN and IVL were detected via quantitative PCR. The data were normalized to internal GAPDH or β-Actin gene expression. The data are expressed as means ± SD of 3 independent experiments performed in duplicate. # p < 0.05, ## p < 0.01, ### p < 0.001 vs. the nonstimulated group; * p < 0.05, ** p < 0.01, and *** p < 0.001 vs. the vehicle group.
    Hacat Cells, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hy-n2909/Aurantiamide/pmc12176770-92-0-25
    Average 94 stars, based on 1 article reviews
    hacat cells - by Bioz Stars, 2026-10
    94/100 stars

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    1) Product Images from "Aqueous extracts of Portulaca oleracea L. alleviate atopic dermatitis by restoring skin barrier function"

    Article Title: Aqueous extracts of Portulaca oleracea L. alleviate atopic dermatitis by restoring skin barrier function

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2025.1591394

    Aurantiamide acetate suppresses dermal inflammation and restores skin barrier function through targeting JAK1. (A) Diagram of the molecular docking between aurantiamide acetate, an active ingredient in PO, and JAK1 (PDB: 6BBU). (B) Inhibitory effects of aurantiamide acetate on JAK1 tyrosine kinase activity detected by the ADP-Glo™ reagent. (C) siRNA-JAK1 silencing efficiency 24 h after transfection. (D) Relative mRNA expression levels of IL17A, IL4, IL1β and FLG were detected via quantitative PCR in HaCaT cells transfected with NC or JAK1 siRNA. (E) Aurantiamide acetate inhibits proinflammatory gene transcription in non-siRNA-treated HaCaT keratinocytes stimulated with TNF-α/IFN-γ. (F) Aurantiamide acetate upregulates skin barrier protective gene transcription in non-siRNA-targeted HaCaT keratinocytes stimulated with TNF-α/IFN-γ. (C–F) Cells were pretreated with aurantiamide acetate (25, 50, or 100 μM) or vehicle (0.1% DMSO) for 1 h before TNF-α (10 ng/mL) and IFN-γ (10 ng/mL) challenge for 18 h. Relative mRNA expression levels of IL6 , IL1β , PTGS2 (COX-2) , CCL17 (TARC) , IL8 , IL4 , IL17A , FLG , LORICRIN and IVL were detected via quantitative PCR. The data were normalized to internal GAPDH or β-Actin gene expression. The data are expressed as means ± SD of 3 independent experiments performed in duplicate. # p < 0.05, ## p < 0.01, ### p < 0.001 vs. the nonstimulated group; * p < 0.05, ** p < 0.01, and *** p < 0.001 vs. the vehicle group.
    Figure Legend Snippet: Aurantiamide acetate suppresses dermal inflammation and restores skin barrier function through targeting JAK1. (A) Diagram of the molecular docking between aurantiamide acetate, an active ingredient in PO, and JAK1 (PDB: 6BBU). (B) Inhibitory effects of aurantiamide acetate on JAK1 tyrosine kinase activity detected by the ADP-Glo™ reagent. (C) siRNA-JAK1 silencing efficiency 24 h after transfection. (D) Relative mRNA expression levels of IL17A, IL4, IL1β and FLG were detected via quantitative PCR in HaCaT cells transfected with NC or JAK1 siRNA. (E) Aurantiamide acetate inhibits proinflammatory gene transcription in non-siRNA-treated HaCaT keratinocytes stimulated with TNF-α/IFN-γ. (F) Aurantiamide acetate upregulates skin barrier protective gene transcription in non-siRNA-targeted HaCaT keratinocytes stimulated with TNF-α/IFN-γ. (C–F) Cells were pretreated with aurantiamide acetate (25, 50, or 100 μM) or vehicle (0.1% DMSO) for 1 h before TNF-α (10 ng/mL) and IFN-γ (10 ng/mL) challenge for 18 h. Relative mRNA expression levels of IL6 , IL1β , PTGS2 (COX-2) , CCL17 (TARC) , IL8 , IL4 , IL17A , FLG , LORICRIN and IVL were detected via quantitative PCR. The data were normalized to internal GAPDH or β-Actin gene expression. The data are expressed as means ± SD of 3 independent experiments performed in duplicate. # p < 0.05, ## p < 0.01, ### p < 0.001 vs. the nonstimulated group; * p < 0.05, ** p < 0.01, and *** p < 0.001 vs. the vehicle group.

    Techniques Used: Activity Assay, Transfection, Expressing, Real-time Polymerase Chain Reaction, Gene Expression

    Related Articles

    Viability Assay:

    Article Title: Aqueous extracts of Portulaca oleracea L. alleviate atopic dermatitis by restoring skin barrier function
    Article Snippet: HaCaT keratinocytes were cultured in Dulbecco’s modified Eagle medium (Gibco, Invitrogen, NY, United States) supplemented with 10% fetal bovine serum (Gibco, Invitrogen, NY, United States) and 1% penicillin/streptomycin (Gibco, Invitrogen, NY, United States) at 37°C in a 5% CO 2 incubator. .. HaCaT cells were pretreated with aurantiamide acetate (25, 50, or 100 μM) or vehicle (0.1% DMSO) for 1 h before tumor necrosis factor-alpha (TNF-α, HY-P7058, MCE, United States) and interferon-γ (IFN-γ, HY-P7025, MCE, United States) challenge for 18 h. During the viability assay, the cells were exposed to various concentrations of aurantiamide acetate for 12 h. Cell viability was determined with a Cell Counting Kit-8 (MA0218, MeilunBio, Dalian, China). .. The skin tissue supernatant and serum were used for the measurement of IgE (Lot#JL12885), IL-4 (Lot#JL20266), IFN-γ (Lot#JL10967), and IL-17 (Lot#JL20250) levels via enzyme-linked immunosorbent assay (ELISA) kits (JiangLai, Shanghai, China) according to the manufacturer’s instructions.

    Article Title: Aqueous extracts of Portulaca oleracea L. alleviate atopic dermatitis by restoring skin barrier function
    Article Snippet: HaCaT keratinocytes were cultured in Dulbecco’s modified Eagle medium (Gibco, Invitrogen, NY, United States) supplemented with 10% fetal bovine serum (Gibco, Invitrogen, NY, United States) and 1% penicillin/streptomycin (Gibco, Invitrogen, NY, United States) at 37°C in a 5% CO2 incubator. .. HaCaT cells were pretreated with aurantiamide acetate (25, 50, or 100 μM) or vehicle (0.1% DMSO) for 1 h before tumor necrosis factor-alpha (TNF-α, HY-P7058, MCE, United States) and interferon-γ (IFN-γ, HY-P7025, MCE, United States) challenge for 18 h. During the viability assay, the cells were exposed to various concentrations of aurantiamide acetate for 12 h. Cell viability was determined with a Cell Counting Kit-8 (MA0218, MeilunBio, Dalian, China). .. The skin tissue supernatant and serum were used for the measurement of IgE (Lot#JL12885), IL-4 (Lot#JL20266), IFN-γ (Lot#JL10967), and IL-17 (Lot#JL20250) levels via enzyme-linked immunosorbent assay (ELISA) kits (JiangLai, Shanghai, China) according to the manufacturer’s instructions.

    CCK-8 Assay:

    Article Title: Aqueous extracts of Portulaca oleracea L. alleviate atopic dermatitis by restoring skin barrier function
    Article Snippet: HaCaT keratinocytes were cultured in Dulbecco’s modified Eagle medium (Gibco, Invitrogen, NY, United States) supplemented with 10% fetal bovine serum (Gibco, Invitrogen, NY, United States) and 1% penicillin/streptomycin (Gibco, Invitrogen, NY, United States) at 37°C in a 5% CO 2 incubator. .. HaCaT cells were pretreated with aurantiamide acetate (25, 50, or 100 μM) or vehicle (0.1% DMSO) for 1 h before tumor necrosis factor-alpha (TNF-α, HY-P7058, MCE, United States) and interferon-γ (IFN-γ, HY-P7025, MCE, United States) challenge for 18 h. During the viability assay, the cells were exposed to various concentrations of aurantiamide acetate for 12 h. Cell viability was determined with a Cell Counting Kit-8 (MA0218, MeilunBio, Dalian, China). .. The skin tissue supernatant and serum were used for the measurement of IgE (Lot#JL12885), IL-4 (Lot#JL20266), IFN-γ (Lot#JL10967), and IL-17 (Lot#JL20250) levels via enzyme-linked immunosorbent assay (ELISA) kits (JiangLai, Shanghai, China) according to the manufacturer’s instructions.

    Article Title: Aqueous extracts of Portulaca oleracea L. alleviate atopic dermatitis by restoring skin barrier function
    Article Snippet: HaCaT keratinocytes were cultured in Dulbecco’s modified Eagle medium (Gibco, Invitrogen, NY, United States) supplemented with 10% fetal bovine serum (Gibco, Invitrogen, NY, United States) and 1% penicillin/streptomycin (Gibco, Invitrogen, NY, United States) at 37°C in a 5% CO2 incubator. .. HaCaT cells were pretreated with aurantiamide acetate (25, 50, or 100 μM) or vehicle (0.1% DMSO) for 1 h before tumor necrosis factor-alpha (TNF-α, HY-P7058, MCE, United States) and interferon-γ (IFN-γ, HY-P7025, MCE, United States) challenge for 18 h. During the viability assay, the cells were exposed to various concentrations of aurantiamide acetate for 12 h. Cell viability was determined with a Cell Counting Kit-8 (MA0218, MeilunBio, Dalian, China). .. The skin tissue supernatant and serum were used for the measurement of IgE (Lot#JL12885), IL-4 (Lot#JL20266), IFN-γ (Lot#JL10967), and IL-17 (Lot#JL20250) levels via enzyme-linked immunosorbent assay (ELISA) kits (JiangLai, Shanghai, China) according to the manufacturer’s instructions.



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    94
    MedChemExpress hacat cells
    <t>Aurantiamide</t> acetate suppresses dermal inflammation and restores skin barrier function through targeting JAK1. (A) Diagram of the molecular docking between aurantiamide acetate, an active ingredient in PO, and JAK1 (PDB: 6BBU). (B) Inhibitory effects of aurantiamide acetate on JAK1 tyrosine kinase activity detected by the ADP-Glo™ reagent. (C) siRNA-JAK1 silencing efficiency 24 h after transfection. (D) Relative mRNA expression levels of IL17A, IL4, IL1β and FLG were detected via quantitative PCR in <t>HaCaT</t> cells transfected with NC or JAK1 siRNA. (E) Aurantiamide acetate inhibits proinflammatory gene transcription in non-siRNA-treated HaCaT keratinocytes stimulated with TNF-α/IFN-γ. (F) Aurantiamide acetate upregulates skin barrier protective gene transcription in non-siRNA-targeted HaCaT keratinocytes stimulated with TNF-α/IFN-γ. (C–F) Cells were pretreated with aurantiamide acetate (25, 50, or 100 μM) or vehicle (0.1% DMSO) for 1 h before TNF-α (10 ng/mL) and IFN-γ (10 ng/mL) challenge for 18 h. Relative mRNA expression levels of IL6 , IL1β , PTGS2 (COX-2) , CCL17 (TARC) , IL8 , IL4 , IL17A , FLG , LORICRIN and IVL were detected via quantitative PCR. The data were normalized to internal GAPDH or β-Actin gene expression. The data are expressed as means ± SD of 3 independent experiments performed in duplicate. # p < 0.05, ## p < 0.01, ### p < 0.001 vs. the nonstimulated group; * p < 0.05, ** p < 0.01, and *** p < 0.001 vs. the vehicle group.
    Hacat Cells, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hy-n2909/Aurantiamide/pmc12176770-92-0-25
    Average 94 stars, based on 1 article reviews
    hacat cells - by Bioz Stars, 2026-10
    94/100 stars
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    Aurantiamide acetate suppresses dermal inflammation and restores skin barrier function through targeting JAK1. (A) Diagram of the molecular docking between aurantiamide acetate, an active ingredient in PO, and JAK1 (PDB: 6BBU). (B) Inhibitory effects of aurantiamide acetate on JAK1 tyrosine kinase activity detected by the ADP-Glo™ reagent. (C) siRNA-JAK1 silencing efficiency 24 h after transfection. (D) Relative mRNA expression levels of IL17A, IL4, IL1β and FLG were detected via quantitative PCR in HaCaT cells transfected with NC or JAK1 siRNA. (E) Aurantiamide acetate inhibits proinflammatory gene transcription in non-siRNA-treated HaCaT keratinocytes stimulated with TNF-α/IFN-γ. (F) Aurantiamide acetate upregulates skin barrier protective gene transcription in non-siRNA-targeted HaCaT keratinocytes stimulated with TNF-α/IFN-γ. (C–F) Cells were pretreated with aurantiamide acetate (25, 50, or 100 μM) or vehicle (0.1% DMSO) for 1 h before TNF-α (10 ng/mL) and IFN-γ (10 ng/mL) challenge for 18 h. Relative mRNA expression levels of IL6 , IL1β , PTGS2 (COX-2) , CCL17 (TARC) , IL8 , IL4 , IL17A , FLG , LORICRIN and IVL were detected via quantitative PCR. The data were normalized to internal GAPDH or β-Actin gene expression. The data are expressed as means ± SD of 3 independent experiments performed in duplicate. # p < 0.05, ## p < 0.01, ### p < 0.001 vs. the nonstimulated group; * p < 0.05, ** p < 0.01, and *** p < 0.001 vs. the vehicle group.

    Journal: Frontiers in Pharmacology

    Article Title: Aqueous extracts of Portulaca oleracea L. alleviate atopic dermatitis by restoring skin barrier function

    doi: 10.3389/fphar.2025.1591394

    Figure Lengend Snippet: Aurantiamide acetate suppresses dermal inflammation and restores skin barrier function through targeting JAK1. (A) Diagram of the molecular docking between aurantiamide acetate, an active ingredient in PO, and JAK1 (PDB: 6BBU). (B) Inhibitory effects of aurantiamide acetate on JAK1 tyrosine kinase activity detected by the ADP-Glo™ reagent. (C) siRNA-JAK1 silencing efficiency 24 h after transfection. (D) Relative mRNA expression levels of IL17A, IL4, IL1β and FLG were detected via quantitative PCR in HaCaT cells transfected with NC or JAK1 siRNA. (E) Aurantiamide acetate inhibits proinflammatory gene transcription in non-siRNA-treated HaCaT keratinocytes stimulated with TNF-α/IFN-γ. (F) Aurantiamide acetate upregulates skin barrier protective gene transcription in non-siRNA-targeted HaCaT keratinocytes stimulated with TNF-α/IFN-γ. (C–F) Cells were pretreated with aurantiamide acetate (25, 50, or 100 μM) or vehicle (0.1% DMSO) for 1 h before TNF-α (10 ng/mL) and IFN-γ (10 ng/mL) challenge for 18 h. Relative mRNA expression levels of IL6 , IL1β , PTGS2 (COX-2) , CCL17 (TARC) , IL8 , IL4 , IL17A , FLG , LORICRIN and IVL were detected via quantitative PCR. The data were normalized to internal GAPDH or β-Actin gene expression. The data are expressed as means ± SD of 3 independent experiments performed in duplicate. # p < 0.05, ## p < 0.01, ### p < 0.001 vs. the nonstimulated group; * p < 0.05, ** p < 0.01, and *** p < 0.001 vs. the vehicle group.

    Article Snippet: HaCaT cells were pretreated with aurantiamide acetate (25, 50, or 100 μM) or vehicle (0.1% DMSO) for 1 h before tumor necrosis factor-alpha (TNF-α, HY-P7058, MCE, United States) and interferon-γ (IFN-γ, HY-P7025, MCE, United States) challenge for 18 h. During the viability assay, the cells were exposed to various concentrations of aurantiamide acetate for 12 h. Cell viability was determined with a Cell Counting Kit-8 (MA0218, MeilunBio, Dalian, China).

    Techniques: Activity Assay, Transfection, Expressing, Real-time Polymerase Chain Reaction, Gene Expression