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ag490 group  (MedChemExpress)


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    Structured Review

    MedChemExpress ag490 group
    p-JAK2/JAK2 and p-STAT3/STAT3 were highly expressed in OLP. <t>AG490</t> and RPM inhibited KCs proliferation. AG490 and RPM inhibited homing migration of OLP IELs. (A–C) p-JAK2/JAK2 and p-STAT3/STAT3 were significantly upregulated in OLP compared to controls (n = 6), as detected by western blot. (D) In the MTT assay, at 48 h, the OD450 values of the AG490 group, RPM group, and AG490+RPM group were significantly lower than those of the Control group. Compared with the AG490 group and RPM group, the OD450 values of the AG490+RPM group were significantly reduced. Additionally, the OD450 values of the AG490 group were significantly lower than those of the RPM group. (E) Compared with the control group, the AG490 group and RPM group exhibited a significant reduction in the number of migration tracks, while the AG490+RPM group showed a significantly reduced number of tracks. (F, G) Compared with the control group, the AG490 group and RPM group demonstrated a significant decrease in both speed and maximum displacement, and the AG490+RPM group exhibited a significant reduction in both speed and maximum displacement. * p < 0.05; ** p < 0.01; *** p < 0.001. JAK2, Janus kinase 2; p-JAK2, Phosphorylated Janus kinase 2; STAT3, Signal transducer and activator of transcription 3; p-STAT3, Phosphorylated signal transducer and activator of transcription 3; OD, Optical density; AG490, (E)-N-Benzyl-2-cyano-3-(3,4-dihydroxyphenyl)prop-2-enamide; RPM, Ruxolitinib.
    Ag490 Group, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 96/100, based on 217 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ag490 group/product/MedChemExpress
    Average 96 stars, based on 217 article reviews
    ag490 group - by Bioz Stars, 2026-05
    96/100 stars

    Images

    1) Product Images from "Keratinocytes regulate intraepithelial lymphocytes homing and mediate mucosal barrier integrity via JAK2/STAT3 signaling in oral lichen planus"

    Article Title: Keratinocytes regulate intraepithelial lymphocytes homing and mediate mucosal barrier integrity via JAK2/STAT3 signaling in oral lichen planus

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2026.1794867

    p-JAK2/JAK2 and p-STAT3/STAT3 were highly expressed in OLP. AG490 and RPM inhibited KCs proliferation. AG490 and RPM inhibited homing migration of OLP IELs. (A–C) p-JAK2/JAK2 and p-STAT3/STAT3 were significantly upregulated in OLP compared to controls (n = 6), as detected by western blot. (D) In the MTT assay, at 48 h, the OD450 values of the AG490 group, RPM group, and AG490+RPM group were significantly lower than those of the Control group. Compared with the AG490 group and RPM group, the OD450 values of the AG490+RPM group were significantly reduced. Additionally, the OD450 values of the AG490 group were significantly lower than those of the RPM group. (E) Compared with the control group, the AG490 group and RPM group exhibited a significant reduction in the number of migration tracks, while the AG490+RPM group showed a significantly reduced number of tracks. (F, G) Compared with the control group, the AG490 group and RPM group demonstrated a significant decrease in both speed and maximum displacement, and the AG490+RPM group exhibited a significant reduction in both speed and maximum displacement. * p < 0.05; ** p < 0.01; *** p < 0.001. JAK2, Janus kinase 2; p-JAK2, Phosphorylated Janus kinase 2; STAT3, Signal transducer and activator of transcription 3; p-STAT3, Phosphorylated signal transducer and activator of transcription 3; OD, Optical density; AG490, (E)-N-Benzyl-2-cyano-3-(3,4-dihydroxyphenyl)prop-2-enamide; RPM, Ruxolitinib.
    Figure Legend Snippet: p-JAK2/JAK2 and p-STAT3/STAT3 were highly expressed in OLP. AG490 and RPM inhibited KCs proliferation. AG490 and RPM inhibited homing migration of OLP IELs. (A–C) p-JAK2/JAK2 and p-STAT3/STAT3 were significantly upregulated in OLP compared to controls (n = 6), as detected by western blot. (D) In the MTT assay, at 48 h, the OD450 values of the AG490 group, RPM group, and AG490+RPM group were significantly lower than those of the Control group. Compared with the AG490 group and RPM group, the OD450 values of the AG490+RPM group were significantly reduced. Additionally, the OD450 values of the AG490 group were significantly lower than those of the RPM group. (E) Compared with the control group, the AG490 group and RPM group exhibited a significant reduction in the number of migration tracks, while the AG490+RPM group showed a significantly reduced number of tracks. (F, G) Compared with the control group, the AG490 group and RPM group demonstrated a significant decrease in both speed and maximum displacement, and the AG490+RPM group exhibited a significant reduction in both speed and maximum displacement. * p < 0.05; ** p < 0.01; *** p < 0.001. JAK2, Janus kinase 2; p-JAK2, Phosphorylated Janus kinase 2; STAT3, Signal transducer and activator of transcription 3; p-STAT3, Phosphorylated signal transducer and activator of transcription 3; OD, Optical density; AG490, (E)-N-Benzyl-2-cyano-3-(3,4-dihydroxyphenyl)prop-2-enamide; RPM, Ruxolitinib.

    Techniques Used: Migration, Western Blot, MTT Assay, Control

    AG490 and RPM inhibited the expression of apoptosis-related proteins Bax and caspase-3 and promoted the expression of Bcl-2, as measured by ELISA. (a), compared with control, p < 0.05; (b), compared with AG490 group, p < 0.05; (c), compared with RPM group, p < 0.05. AG490, (E)-N-Benzyl-2-cyano-3-(3,4-dihydroxyphenyl)prop-2-enamide; RPM, Ruxolitinib; Bax, Bcl-2 associated X protein; Bcl-2, B-cell lymphoma/leukemia-2 gene; caspase-3, Cysteine-dependent aspartate-specific protease-3.
    Figure Legend Snippet: AG490 and RPM inhibited the expression of apoptosis-related proteins Bax and caspase-3 and promoted the expression of Bcl-2, as measured by ELISA. (a), compared with control, p < 0.05; (b), compared with AG490 group, p < 0.05; (c), compared with RPM group, p < 0.05. AG490, (E)-N-Benzyl-2-cyano-3-(3,4-dihydroxyphenyl)prop-2-enamide; RPM, Ruxolitinib; Bax, Bcl-2 associated X protein; Bcl-2, B-cell lymphoma/leukemia-2 gene; caspase-3, Cysteine-dependent aspartate-specific protease-3.

    Techniques Used: Expressing, Enzyme-linked Immunosorbent Assay, Control

    AG490 and RPM synergistically inhibited the phosphorylation of JAK2/STAT3. (A, B) AG490 and RPM selectively inhibited JAK2/STAT3 phosphorylation. * p < 0.05; ** p < 0.01; *** p < 0.001. (C) JAK2 and p-JAK2 were downregulated in AG490 and AG490+RPM group. (D) STAT3 and p-STAT3 were downregulated in RPM and AG490+RPM group. (E) Compared with the control group, the protein ratios of p-JAK2/JAK2 and p-STAT3/STAT3 were significantly increased in the AG490 group, RPM group, and AG490+RPM group. Compared with the AG490 group and RPM group, the protein ratios of p-JAK2/JAK2 and p-STAT3/STAT3 were significantly decreased in the AG490+RPM group. a, compared with control, p < 0.05; b, compared with AG490 group, p < 0.05; c, compared with RPM group, p < 0.05; aa, compared with control, p < 0.01. AG490, (E)-N-Benzyl-2-cyano-3-(3,4-dihydroxyphenyl)prop-2-enamide; RPM, Ruxolitinib; JAK2, Janus kinase 2; p-JAK2, Phosphorylated Janus kinase 2; STAT3, Signal transducer and activator of transcription 3; p-STAT3: Phosphorylated signal transducer and activator of transcription 3; GAPDH, Glycerol-3-phosphate dehydrogenase.
    Figure Legend Snippet: AG490 and RPM synergistically inhibited the phosphorylation of JAK2/STAT3. (A, B) AG490 and RPM selectively inhibited JAK2/STAT3 phosphorylation. * p < 0.05; ** p < 0.01; *** p < 0.001. (C) JAK2 and p-JAK2 were downregulated in AG490 and AG490+RPM group. (D) STAT3 and p-STAT3 were downregulated in RPM and AG490+RPM group. (E) Compared with the control group, the protein ratios of p-JAK2/JAK2 and p-STAT3/STAT3 were significantly increased in the AG490 group, RPM group, and AG490+RPM group. Compared with the AG490 group and RPM group, the protein ratios of p-JAK2/JAK2 and p-STAT3/STAT3 were significantly decreased in the AG490+RPM group. a, compared with control, p < 0.05; b, compared with AG490 group, p < 0.05; c, compared with RPM group, p < 0.05; aa, compared with control, p < 0.01. AG490, (E)-N-Benzyl-2-cyano-3-(3,4-dihydroxyphenyl)prop-2-enamide; RPM, Ruxolitinib; JAK2, Janus kinase 2; p-JAK2, Phosphorylated Janus kinase 2; STAT3, Signal transducer and activator of transcription 3; p-STAT3: Phosphorylated signal transducer and activator of transcription 3; GAPDH, Glycerol-3-phosphate dehydrogenase.

    Techniques Used: Phospho-proteomics, Control

    The expression of ZO-1 and Occludin mRNA was upregulated after using AG490 and RPM. (A, B) Compared with the control group, the expression of ZO-1 and Occludin mRNA increased in the AG490 group. The expression of ZO-1 and Occludin mRAN in the RPM group was upregulated. The expression of ZO-1 and Occludin mRNA was significantly increased in the AG490+RPM group. Compared with the RPM group, the AG490+RPM group showed increased expression of ZO-1 and Occludin mRNA. * p < 0.05; ** p < 0.01; *** p < 0.001. (C) Schematic diagram of the regulatory network mechanism involving E-cadherin/CD103-JAK2/STAT3-ZO-1/Occludin in OLP. The binding of E-cadherin/CD103 downregulated JAK2/STAT3 phosphorylation in KCs and upregulated mucosal barrier molecules ZO-1 and Occludin, which helped maintain the integrity of the mucosal barrier. CD103, Integrin alpha-E; E-cadherin, Epithelial cadherin; JAK2, Janus kinase 2; STAT3, Signal transducer and activator of transcription 3; AG490, (E)-N-Benzyl-2-cyano-3-(3,4-dihydroxyphenyl)prop-2-enamide; RPM, Ruxolitinib; ZO-1, Zonula occludens protein 1; KC, Keratinocytes; IEL, Intraepithelial lymphocyte.
    Figure Legend Snippet: The expression of ZO-1 and Occludin mRNA was upregulated after using AG490 and RPM. (A, B) Compared with the control group, the expression of ZO-1 and Occludin mRNA increased in the AG490 group. The expression of ZO-1 and Occludin mRAN in the RPM group was upregulated. The expression of ZO-1 and Occludin mRNA was significantly increased in the AG490+RPM group. Compared with the RPM group, the AG490+RPM group showed increased expression of ZO-1 and Occludin mRNA. * p < 0.05; ** p < 0.01; *** p < 0.001. (C) Schematic diagram of the regulatory network mechanism involving E-cadherin/CD103-JAK2/STAT3-ZO-1/Occludin in OLP. The binding of E-cadherin/CD103 downregulated JAK2/STAT3 phosphorylation in KCs and upregulated mucosal barrier molecules ZO-1 and Occludin, which helped maintain the integrity of the mucosal barrier. CD103, Integrin alpha-E; E-cadherin, Epithelial cadherin; JAK2, Janus kinase 2; STAT3, Signal transducer and activator of transcription 3; AG490, (E)-N-Benzyl-2-cyano-3-(3,4-dihydroxyphenyl)prop-2-enamide; RPM, Ruxolitinib; ZO-1, Zonula occludens protein 1; KC, Keratinocytes; IEL, Intraepithelial lymphocyte.

    Techniques Used: Expressing, Control, Binding Assay, Phospho-proteomics



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    p-JAK2/JAK2 and p-STAT3/STAT3 were highly expressed in OLP. <t>AG490</t> and RPM inhibited KCs proliferation. AG490 and RPM inhibited homing migration of OLP IELs. (A–C) p-JAK2/JAK2 and p-STAT3/STAT3 were significantly upregulated in OLP compared to controls (n = 6), as detected by western blot. (D) In the MTT assay, at 48 h, the OD450 values of the AG490 group, RPM group, and AG490+RPM group were significantly lower than those of the Control group. Compared with the AG490 group and RPM group, the OD450 values of the AG490+RPM group were significantly reduced. Additionally, the OD450 values of the AG490 group were significantly lower than those of the RPM group. (E) Compared with the control group, the AG490 group and RPM group exhibited a significant reduction in the number of migration tracks, while the AG490+RPM group showed a significantly reduced number of tracks. (F, G) Compared with the control group, the AG490 group and RPM group demonstrated a significant decrease in both speed and maximum displacement, and the AG490+RPM group exhibited a significant reduction in both speed and maximum displacement. * p < 0.05; ** p < 0.01; *** p < 0.001. JAK2, Janus kinase 2; p-JAK2, Phosphorylated Janus kinase 2; STAT3, Signal transducer and activator of transcription 3; p-STAT3, Phosphorylated signal transducer and activator of transcription 3; OD, Optical density; AG490, (E)-N-Benzyl-2-cyano-3-(3,4-dihydroxyphenyl)prop-2-enamide; RPM, Ruxolitinib.
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    Image Search Results


    p-JAK2/JAK2 and p-STAT3/STAT3 were highly expressed in OLP. AG490 and RPM inhibited KCs proliferation. AG490 and RPM inhibited homing migration of OLP IELs. (A–C) p-JAK2/JAK2 and p-STAT3/STAT3 were significantly upregulated in OLP compared to controls (n = 6), as detected by western blot. (D) In the MTT assay, at 48 h, the OD450 values of the AG490 group, RPM group, and AG490+RPM group were significantly lower than those of the Control group. Compared with the AG490 group and RPM group, the OD450 values of the AG490+RPM group were significantly reduced. Additionally, the OD450 values of the AG490 group were significantly lower than those of the RPM group. (E) Compared with the control group, the AG490 group and RPM group exhibited a significant reduction in the number of migration tracks, while the AG490+RPM group showed a significantly reduced number of tracks. (F, G) Compared with the control group, the AG490 group and RPM group demonstrated a significant decrease in both speed and maximum displacement, and the AG490+RPM group exhibited a significant reduction in both speed and maximum displacement. * p < 0.05; ** p < 0.01; *** p < 0.001. JAK2, Janus kinase 2; p-JAK2, Phosphorylated Janus kinase 2; STAT3, Signal transducer and activator of transcription 3; p-STAT3, Phosphorylated signal transducer and activator of transcription 3; OD, Optical density; AG490, (E)-N-Benzyl-2-cyano-3-(3,4-dihydroxyphenyl)prop-2-enamide; RPM, Ruxolitinib.

    Journal: Frontiers in Immunology

    Article Title: Keratinocytes regulate intraepithelial lymphocytes homing and mediate mucosal barrier integrity via JAK2/STAT3 signaling in oral lichen planus

    doi: 10.3389/fimmu.2026.1794867

    Figure Lengend Snippet: p-JAK2/JAK2 and p-STAT3/STAT3 were highly expressed in OLP. AG490 and RPM inhibited KCs proliferation. AG490 and RPM inhibited homing migration of OLP IELs. (A–C) p-JAK2/JAK2 and p-STAT3/STAT3 were significantly upregulated in OLP compared to controls (n = 6), as detected by western blot. (D) In the MTT assay, at 48 h, the OD450 values of the AG490 group, RPM group, and AG490+RPM group were significantly lower than those of the Control group. Compared with the AG490 group and RPM group, the OD450 values of the AG490+RPM group were significantly reduced. Additionally, the OD450 values of the AG490 group were significantly lower than those of the RPM group. (E) Compared with the control group, the AG490 group and RPM group exhibited a significant reduction in the number of migration tracks, while the AG490+RPM group showed a significantly reduced number of tracks. (F, G) Compared with the control group, the AG490 group and RPM group demonstrated a significant decrease in both speed and maximum displacement, and the AG490+RPM group exhibited a significant reduction in both speed and maximum displacement. * p < 0.05; ** p < 0.01; *** p < 0.001. JAK2, Janus kinase 2; p-JAK2, Phosphorylated Janus kinase 2; STAT3, Signal transducer and activator of transcription 3; p-STAT3, Phosphorylated signal transducer and activator of transcription 3; OD, Optical density; AG490, (E)-N-Benzyl-2-cyano-3-(3,4-dihydroxyphenyl)prop-2-enamide; RPM, Ruxolitinib.

    Article Snippet: The models were divided into four groups based on the addition of inhibitors: (1) Control group (treated with K-SFM medium containing an equal concentration of PBS); (2) AG490 group (treated with K-SFM medium containing 50 μmol/L AG490) (AG490, Cat # HY-12003, MCE); (3) RPM group (treated with K-SFM medium containing 20 nmol/L RPM) (RPM, Cat # HY-10219, MCE); and (4) AG490+RPM group (treated with K-SFM medium containing 50 μmol/L AG490 and 20 nmol/L RPM).

    Techniques: Migration, Western Blot, MTT Assay, Control

    AG490 and RPM inhibited the expression of apoptosis-related proteins Bax and caspase-3 and promoted the expression of Bcl-2, as measured by ELISA. (a), compared with control, p < 0.05; (b), compared with AG490 group, p < 0.05; (c), compared with RPM group, p < 0.05. AG490, (E)-N-Benzyl-2-cyano-3-(3,4-dihydroxyphenyl)prop-2-enamide; RPM, Ruxolitinib; Bax, Bcl-2 associated X protein; Bcl-2, B-cell lymphoma/leukemia-2 gene; caspase-3, Cysteine-dependent aspartate-specific protease-3.

    Journal: Frontiers in Immunology

    Article Title: Keratinocytes regulate intraepithelial lymphocytes homing and mediate mucosal barrier integrity via JAK2/STAT3 signaling in oral lichen planus

    doi: 10.3389/fimmu.2026.1794867

    Figure Lengend Snippet: AG490 and RPM inhibited the expression of apoptosis-related proteins Bax and caspase-3 and promoted the expression of Bcl-2, as measured by ELISA. (a), compared with control, p < 0.05; (b), compared with AG490 group, p < 0.05; (c), compared with RPM group, p < 0.05. AG490, (E)-N-Benzyl-2-cyano-3-(3,4-dihydroxyphenyl)prop-2-enamide; RPM, Ruxolitinib; Bax, Bcl-2 associated X protein; Bcl-2, B-cell lymphoma/leukemia-2 gene; caspase-3, Cysteine-dependent aspartate-specific protease-3.

    Article Snippet: The models were divided into four groups based on the addition of inhibitors: (1) Control group (treated with K-SFM medium containing an equal concentration of PBS); (2) AG490 group (treated with K-SFM medium containing 50 μmol/L AG490) (AG490, Cat # HY-12003, MCE); (3) RPM group (treated with K-SFM medium containing 20 nmol/L RPM) (RPM, Cat # HY-10219, MCE); and (4) AG490+RPM group (treated with K-SFM medium containing 50 μmol/L AG490 and 20 nmol/L RPM).

    Techniques: Expressing, Enzyme-linked Immunosorbent Assay, Control

    AG490 and RPM synergistically inhibited the phosphorylation of JAK2/STAT3. (A, B) AG490 and RPM selectively inhibited JAK2/STAT3 phosphorylation. * p < 0.05; ** p < 0.01; *** p < 0.001. (C) JAK2 and p-JAK2 were downregulated in AG490 and AG490+RPM group. (D) STAT3 and p-STAT3 were downregulated in RPM and AG490+RPM group. (E) Compared with the control group, the protein ratios of p-JAK2/JAK2 and p-STAT3/STAT3 were significantly increased in the AG490 group, RPM group, and AG490+RPM group. Compared with the AG490 group and RPM group, the protein ratios of p-JAK2/JAK2 and p-STAT3/STAT3 were significantly decreased in the AG490+RPM group. a, compared with control, p < 0.05; b, compared with AG490 group, p < 0.05; c, compared with RPM group, p < 0.05; aa, compared with control, p < 0.01. AG490, (E)-N-Benzyl-2-cyano-3-(3,4-dihydroxyphenyl)prop-2-enamide; RPM, Ruxolitinib; JAK2, Janus kinase 2; p-JAK2, Phosphorylated Janus kinase 2; STAT3, Signal transducer and activator of transcription 3; p-STAT3: Phosphorylated signal transducer and activator of transcription 3; GAPDH, Glycerol-3-phosphate dehydrogenase.

    Journal: Frontiers in Immunology

    Article Title: Keratinocytes regulate intraepithelial lymphocytes homing and mediate mucosal barrier integrity via JAK2/STAT3 signaling in oral lichen planus

    doi: 10.3389/fimmu.2026.1794867

    Figure Lengend Snippet: AG490 and RPM synergistically inhibited the phosphorylation of JAK2/STAT3. (A, B) AG490 and RPM selectively inhibited JAK2/STAT3 phosphorylation. * p < 0.05; ** p < 0.01; *** p < 0.001. (C) JAK2 and p-JAK2 were downregulated in AG490 and AG490+RPM group. (D) STAT3 and p-STAT3 were downregulated in RPM and AG490+RPM group. (E) Compared with the control group, the protein ratios of p-JAK2/JAK2 and p-STAT3/STAT3 were significantly increased in the AG490 group, RPM group, and AG490+RPM group. Compared with the AG490 group and RPM group, the protein ratios of p-JAK2/JAK2 and p-STAT3/STAT3 were significantly decreased in the AG490+RPM group. a, compared with control, p < 0.05; b, compared with AG490 group, p < 0.05; c, compared with RPM group, p < 0.05; aa, compared with control, p < 0.01. AG490, (E)-N-Benzyl-2-cyano-3-(3,4-dihydroxyphenyl)prop-2-enamide; RPM, Ruxolitinib; JAK2, Janus kinase 2; p-JAK2, Phosphorylated Janus kinase 2; STAT3, Signal transducer and activator of transcription 3; p-STAT3: Phosphorylated signal transducer and activator of transcription 3; GAPDH, Glycerol-3-phosphate dehydrogenase.

    Article Snippet: The models were divided into four groups based on the addition of inhibitors: (1) Control group (treated with K-SFM medium containing an equal concentration of PBS); (2) AG490 group (treated with K-SFM medium containing 50 μmol/L AG490) (AG490, Cat # HY-12003, MCE); (3) RPM group (treated with K-SFM medium containing 20 nmol/L RPM) (RPM, Cat # HY-10219, MCE); and (4) AG490+RPM group (treated with K-SFM medium containing 50 μmol/L AG490 and 20 nmol/L RPM).

    Techniques: Phospho-proteomics, Control

    The expression of ZO-1 and Occludin mRNA was upregulated after using AG490 and RPM. (A, B) Compared with the control group, the expression of ZO-1 and Occludin mRNA increased in the AG490 group. The expression of ZO-1 and Occludin mRAN in the RPM group was upregulated. The expression of ZO-1 and Occludin mRNA was significantly increased in the AG490+RPM group. Compared with the RPM group, the AG490+RPM group showed increased expression of ZO-1 and Occludin mRNA. * p < 0.05; ** p < 0.01; *** p < 0.001. (C) Schematic diagram of the regulatory network mechanism involving E-cadherin/CD103-JAK2/STAT3-ZO-1/Occludin in OLP. The binding of E-cadherin/CD103 downregulated JAK2/STAT3 phosphorylation in KCs and upregulated mucosal barrier molecules ZO-1 and Occludin, which helped maintain the integrity of the mucosal barrier. CD103, Integrin alpha-E; E-cadherin, Epithelial cadherin; JAK2, Janus kinase 2; STAT3, Signal transducer and activator of transcription 3; AG490, (E)-N-Benzyl-2-cyano-3-(3,4-dihydroxyphenyl)prop-2-enamide; RPM, Ruxolitinib; ZO-1, Zonula occludens protein 1; KC, Keratinocytes; IEL, Intraepithelial lymphocyte.

    Journal: Frontiers in Immunology

    Article Title: Keratinocytes regulate intraepithelial lymphocytes homing and mediate mucosal barrier integrity via JAK2/STAT3 signaling in oral lichen planus

    doi: 10.3389/fimmu.2026.1794867

    Figure Lengend Snippet: The expression of ZO-1 and Occludin mRNA was upregulated after using AG490 and RPM. (A, B) Compared with the control group, the expression of ZO-1 and Occludin mRNA increased in the AG490 group. The expression of ZO-1 and Occludin mRAN in the RPM group was upregulated. The expression of ZO-1 and Occludin mRNA was significantly increased in the AG490+RPM group. Compared with the RPM group, the AG490+RPM group showed increased expression of ZO-1 and Occludin mRNA. * p < 0.05; ** p < 0.01; *** p < 0.001. (C) Schematic diagram of the regulatory network mechanism involving E-cadherin/CD103-JAK2/STAT3-ZO-1/Occludin in OLP. The binding of E-cadherin/CD103 downregulated JAK2/STAT3 phosphorylation in KCs and upregulated mucosal barrier molecules ZO-1 and Occludin, which helped maintain the integrity of the mucosal barrier. CD103, Integrin alpha-E; E-cadherin, Epithelial cadherin; JAK2, Janus kinase 2; STAT3, Signal transducer and activator of transcription 3; AG490, (E)-N-Benzyl-2-cyano-3-(3,4-dihydroxyphenyl)prop-2-enamide; RPM, Ruxolitinib; ZO-1, Zonula occludens protein 1; KC, Keratinocytes; IEL, Intraepithelial lymphocyte.

    Article Snippet: The models were divided into four groups based on the addition of inhibitors: (1) Control group (treated with K-SFM medium containing an equal concentration of PBS); (2) AG490 group (treated with K-SFM medium containing 50 μmol/L AG490) (AG490, Cat # HY-12003, MCE); (3) RPM group (treated with K-SFM medium containing 20 nmol/L RPM) (RPM, Cat # HY-10219, MCE); and (4) AG490+RPM group (treated with K-SFM medium containing 50 μmol/L AG490 and 20 nmol/L RPM).

    Techniques: Expressing, Control, Binding Assay, Phospho-proteomics

    PGE1 participates in severe pneumonia by regulating JAK-STAT pathway. A Volcano plot showed the DEGs between the LPS and LPS + PGE1 groups; B Bubble plot from KEGG and GO analyses showed the major enrichment of up-regulated DEGs; C Bubble plot from KEGG and GO analyses showed the major enrichment of down-regulated DEGs; D GSEA-KEGG showed the enrichment of gene-related signaling pathways; E Heatmap showed JAK-STAT pathway-related gene expression between the two groups

    Journal: BMC Pulmonary Medicine

    Article Title: Transcriptomics reveals the underlying mechanism of Prostaglandin E1 in improving severe pneumonia

    doi: 10.1186/s12890-025-03847-y

    Figure Lengend Snippet: PGE1 participates in severe pneumonia by regulating JAK-STAT pathway. A Volcano plot showed the DEGs between the LPS and LPS + PGE1 groups; B Bubble plot from KEGG and GO analyses showed the major enrichment of up-regulated DEGs; C Bubble plot from KEGG and GO analyses showed the major enrichment of down-regulated DEGs; D GSEA-KEGG showed the enrichment of gene-related signaling pathways; E Heatmap showed JAK-STAT pathway-related gene expression between the two groups

    Article Snippet: The tongue and the nose were loosened after 20 s, and then the mice were placed in a cage and allowed to awaken naturally to construct severe pneumonia models [ ]; (3) PGE1 intervention group (LPS + PGE1): after LPS treatment, the mice were also administered 10 mg/kg PGE1 intraperitoneally once a day for 4 d; (4) Dimethyl sulfoxide (DMSO) group (LPS + PGE1 + DMSO): After LPS and PGE1 treatment, the mice were also injected intraperitoneally with an equal dose of 0.1% DMSO in PBS solution; (5) JAK inhibitor group (LPS + PGE1 + AG490): After LPS and PGE1 treatment, the mice were also intraperitoneally injected with 1 mg/kg AG490 (HY-12000, MedChemExpress).

    Techniques: Protein-Protein interactions, Gene Expression

    Combination of PGE1 and JAK inhibitor can regulate the phenotype of mice with severe pneumonia. A H&E staining showed the pathological changes in mouse lung tissues; B W/D values of mouse lung tissues; C ELISA showed the levels of IL-1β, IL-6, IL-10, and TNF-α in mouse BALF and lung tissues; D The number of WBCs and PMNs in mouse BALF; and E Blood gas analyzer detected the PaO 2 and PaCO 2 of mice. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

    Journal: BMC Pulmonary Medicine

    Article Title: Transcriptomics reveals the underlying mechanism of Prostaglandin E1 in improving severe pneumonia

    doi: 10.1186/s12890-025-03847-y

    Figure Lengend Snippet: Combination of PGE1 and JAK inhibitor can regulate the phenotype of mice with severe pneumonia. A H&E staining showed the pathological changes in mouse lung tissues; B W/D values of mouse lung tissues; C ELISA showed the levels of IL-1β, IL-6, IL-10, and TNF-α in mouse BALF and lung tissues; D The number of WBCs and PMNs in mouse BALF; and E Blood gas analyzer detected the PaO 2 and PaCO 2 of mice. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

    Article Snippet: The tongue and the nose were loosened after 20 s, and then the mice were placed in a cage and allowed to awaken naturally to construct severe pneumonia models [ ]; (3) PGE1 intervention group (LPS + PGE1): after LPS treatment, the mice were also administered 10 mg/kg PGE1 intraperitoneally once a day for 4 d; (4) Dimethyl sulfoxide (DMSO) group (LPS + PGE1 + DMSO): After LPS and PGE1 treatment, the mice were also injected intraperitoneally with an equal dose of 0.1% DMSO in PBS solution; (5) JAK inhibitor group (LPS + PGE1 + AG490): After LPS and PGE1 treatment, the mice were also intraperitoneally injected with 1 mg/kg AG490 (HY-12000, MedChemExpress).

    Techniques: Staining, Enzyme-linked Immunosorbent Assay

    Combination of PGE1 and JAK inhibitor can regulate Th17/Treg balance in mice with severe pneumonia. A Flow cytometry detected the ratios of Th17 and Treg cells; B qPCR detected RORγt and Foxp3 mRNA expression. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

    Journal: BMC Pulmonary Medicine

    Article Title: Transcriptomics reveals the underlying mechanism of Prostaglandin E1 in improving severe pneumonia

    doi: 10.1186/s12890-025-03847-y

    Figure Lengend Snippet: Combination of PGE1 and JAK inhibitor can regulate Th17/Treg balance in mice with severe pneumonia. A Flow cytometry detected the ratios of Th17 and Treg cells; B qPCR detected RORγt and Foxp3 mRNA expression. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

    Article Snippet: The tongue and the nose were loosened after 20 s, and then the mice were placed in a cage and allowed to awaken naturally to construct severe pneumonia models [ ]; (3) PGE1 intervention group (LPS + PGE1): after LPS treatment, the mice were also administered 10 mg/kg PGE1 intraperitoneally once a day for 4 d; (4) Dimethyl sulfoxide (DMSO) group (LPS + PGE1 + DMSO): After LPS and PGE1 treatment, the mice were also injected intraperitoneally with an equal dose of 0.1% DMSO in PBS solution; (5) JAK inhibitor group (LPS + PGE1 + AG490): After LPS and PGE1 treatment, the mice were also intraperitoneally injected with 1 mg/kg AG490 (HY-12000, MedChemExpress).

    Techniques: Flow Cytometry, Expressing

    Fig. 5 SPRC inhibited the JAK/STAT signaling pathway in vitro. (A) GSEA revealed significant enrichment of the JAK/STAT signaling pathway. (B-C) Western blot analysis of phosphorylated STAT3 (p-STAT3), total STAT3, phosphorylated JAK2 (p-JAK2), and total JAK2. (D) RT-qPCR analysis of Inos expression. (E-F) Western blot analysis of iNOS protein levels. The data were analyzed via one-way ANOVA (n ≥ 3). Statistical significance is denoted as follows: ###p < 0.001 compared with the control group; *p < 0.05, **p < 0.01, ***p < 0.001 compared with the LPS group; &&&p < 0.001 compared with the LPS + AG490 group

    Journal: Molecular medicine (Cambridge, Mass.)

    Article Title: S-propargyl-cysteine attenuates temporomandibular joint osteoarthritis by regulating macrophage polarization via Inhibition of JAK/STAT signaling.

    doi: 10.1186/s10020-025-01186-6

    Figure Lengend Snippet: Fig. 5 SPRC inhibited the JAK/STAT signaling pathway in vitro. (A) GSEA revealed significant enrichment of the JAK/STAT signaling pathway. (B-C) Western blot analysis of phosphorylated STAT3 (p-STAT3), total STAT3, phosphorylated JAK2 (p-JAK2), and total JAK2. (D) RT-qPCR analysis of Inos expression. (E-F) Western blot analysis of iNOS protein levels. The data were analyzed via one-way ANOVA (n ≥ 3). Statistical significance is denoted as follows: ###p < 0.001 compared with the control group; *p < 0.05, **p < 0.01, ***p < 0.001 compared with the LPS group; &&&p < 0.001 compared with the LPS + AG490 group

    Article Snippet: In the LPS + AG490 group, cells were pretreated with 50 μM AG490 (MedChemExpress, HY-12000, USA) for 1 h, followed by stimulation with LPS for 24 h. In the LPS + SPRC + AG490 group, cells were pretreated with 50 μM AG490 and 100 μM SPRC for 1 h and then stimulated with LPS for 24 h. Rat primary condylar chondrocytes (rPCCs) extraction and culture Rat primary condylar chondrocytes (rPCCs) were isolated from 3-week-old female Sprague-Dawley (SD) rats obtained from the Guangdong Medical Laboratory Animal Center, following a previously established protocol (Yang et al. 2024a, b).

    Techniques: In Vitro, Western Blot, Quantitative RT-PCR, Expressing, Control