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p jak2  (Bioss)


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    Structured Review

    Bioss p jak2
    Naringin inhibits <t>JAK2/STAT3</t> signaling and restores tight junction proteins in dextran sulfate sodium-induced colitis. (A) Representative western blotting images of p-JAK2, JAK2, p-STAT3, STAT3, IL-6, occludin, ZO-1 and β-actin expression in colon tissues. Densitometric semi-quantification of the relative protein expression levels of (B) p-JAK2/β-actin, (C) JAK2/β-actin, (D) p-JAK2/JAK2, (E) p-STAT3/β-actin, (F) STAT3/β-actin, (G) p-STAT3/STAT3, (H) IL-6/β-actin, (I) occludin/β-actin and (J) ZO-1/β-actin. Data are presented as mean ± SEM. n=3. *P<0.05 and **P<0.01 vs. control group; # P<0.05 and ## P<0.01 vs. normal group. One-way ANOVA followed by Tukey's post-hoc test was applied. N, normal group; C, control group; Nar, naringin group; Mes, mesalazine group; p-, phosphorylated; JAK2, Janus kinase 2; STAT3, signal transducer and activator of transcription 3; IL-6, ZO-1, zona occludens-1.
    P Jak2, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 19 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Naringin ameliorates intestinal injury in ulcerative colitis model mice by modulating the JAK2/STAT3 signaling pathway"

    Article Title: Naringin ameliorates intestinal injury in ulcerative colitis model mice by modulating the JAK2/STAT3 signaling pathway

    Journal: Molecular Medicine Reports

    doi: 10.3892/mmr.2026.13805

    Naringin inhibits JAK2/STAT3 signaling and restores tight junction proteins in dextran sulfate sodium-induced colitis. (A) Representative western blotting images of p-JAK2, JAK2, p-STAT3, STAT3, IL-6, occludin, ZO-1 and β-actin expression in colon tissues. Densitometric semi-quantification of the relative protein expression levels of (B) p-JAK2/β-actin, (C) JAK2/β-actin, (D) p-JAK2/JAK2, (E) p-STAT3/β-actin, (F) STAT3/β-actin, (G) p-STAT3/STAT3, (H) IL-6/β-actin, (I) occludin/β-actin and (J) ZO-1/β-actin. Data are presented as mean ± SEM. n=3. *P<0.05 and **P<0.01 vs. control group; # P<0.05 and ## P<0.01 vs. normal group. One-way ANOVA followed by Tukey's post-hoc test was applied. N, normal group; C, control group; Nar, naringin group; Mes, mesalazine group; p-, phosphorylated; JAK2, Janus kinase 2; STAT3, signal transducer and activator of transcription 3; IL-6, ZO-1, zona occludens-1.
    Figure Legend Snippet: Naringin inhibits JAK2/STAT3 signaling and restores tight junction proteins in dextran sulfate sodium-induced colitis. (A) Representative western blotting images of p-JAK2, JAK2, p-STAT3, STAT3, IL-6, occludin, ZO-1 and β-actin expression in colon tissues. Densitometric semi-quantification of the relative protein expression levels of (B) p-JAK2/β-actin, (C) JAK2/β-actin, (D) p-JAK2/JAK2, (E) p-STAT3/β-actin, (F) STAT3/β-actin, (G) p-STAT3/STAT3, (H) IL-6/β-actin, (I) occludin/β-actin and (J) ZO-1/β-actin. Data are presented as mean ± SEM. n=3. *P<0.05 and **P<0.01 vs. control group; # P<0.05 and ## P<0.01 vs. normal group. One-way ANOVA followed by Tukey's post-hoc test was applied. N, normal group; C, control group; Nar, naringin group; Mes, mesalazine group; p-, phosphorylated; JAK2, Janus kinase 2; STAT3, signal transducer and activator of transcription 3; IL-6, ZO-1, zona occludens-1.

    Techniques Used: Western Blot, Expressing, Control

    Naringin suppresses JAK2/STAT3 activation in IL-6-stimulated Caco-2 cells with STAT3 silencing. (A) Western blot analysis of p-JAK2, JAK2, p-STAT3, STAT3, occludin and ZO-1 in Caco-2 cells under indicated treatments. (B) Validation of STAT3 knockdown efficiency: Relative STAT3 expression in cells transfected with siSTAT3 vs. siNC. ## P<0.01 vs. siNC. Densitometric semi-quantification of relative protein expression levels of (C) p-JAK2/β-actin, (D) JAK2/β-actin, (E) p-JAK2/JAK2, (F) p-STAT3/β-actin, (G) STAT3/β-actin, (H) p-STAT3/ STAT3, (I) occludin/β-actin, (J) ZO-1/β-actin. Data are presented as mean ± SEM. n=3. *P<0.05 and **P<0.01 vs. IL-6 group; ## P<0.01 vs. normal group; Δ P<0.05 and ΔΔ P<0.01 IL-6 + Nar group vs. IL-6 + Nar + siSTAT3 group. One-way ANOVA followed by Tukey's post-hoc test was applied. N, normal group; Nar, naringin group; Mes, mesalazine group; p-, phosphorylated; JAK2, Janus kinase 2; STAT3, signal transducer and activator of transcription 3; ZO-1, zona occludens-1; si, small interfering RNA; NC, negative control.
    Figure Legend Snippet: Naringin suppresses JAK2/STAT3 activation in IL-6-stimulated Caco-2 cells with STAT3 silencing. (A) Western blot analysis of p-JAK2, JAK2, p-STAT3, STAT3, occludin and ZO-1 in Caco-2 cells under indicated treatments. (B) Validation of STAT3 knockdown efficiency: Relative STAT3 expression in cells transfected with siSTAT3 vs. siNC. ## P<0.01 vs. siNC. Densitometric semi-quantification of relative protein expression levels of (C) p-JAK2/β-actin, (D) JAK2/β-actin, (E) p-JAK2/JAK2, (F) p-STAT3/β-actin, (G) STAT3/β-actin, (H) p-STAT3/ STAT3, (I) occludin/β-actin, (J) ZO-1/β-actin. Data are presented as mean ± SEM. n=3. *P<0.05 and **P<0.01 vs. IL-6 group; ## P<0.01 vs. normal group; Δ P<0.05 and ΔΔ P<0.01 IL-6 + Nar group vs. IL-6 + Nar + siSTAT3 group. One-way ANOVA followed by Tukey's post-hoc test was applied. N, normal group; Nar, naringin group; Mes, mesalazine group; p-, phosphorylated; JAK2, Janus kinase 2; STAT3, signal transducer and activator of transcription 3; ZO-1, zona occludens-1; si, small interfering RNA; NC, negative control.

    Techniques Used: Activation Assay, Western Blot, Biomarker Discovery, Knockdown, Expressing, Transfection, Small Interfering RNA, Negative Control



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    Naringin inhibits <t>JAK2/STAT3</t> signaling and restores tight junction proteins in dextran sulfate sodium-induced colitis. (A) Representative western blotting images of p-JAK2, JAK2, p-STAT3, STAT3, IL-6, occludin, ZO-1 and β-actin expression in colon tissues. Densitometric semi-quantification of the relative protein expression levels of (B) p-JAK2/β-actin, (C) JAK2/β-actin, (D) p-JAK2/JAK2, (E) p-STAT3/β-actin, (F) STAT3/β-actin, (G) p-STAT3/STAT3, (H) IL-6/β-actin, (I) occludin/β-actin and (J) ZO-1/β-actin. Data are presented as mean ± SEM. n=3. *P<0.05 and **P<0.01 vs. control group; # P<0.05 and ## P<0.01 vs. normal group. One-way ANOVA followed by Tukey's post-hoc test was applied. N, normal group; C, control group; Nar, naringin group; Mes, mesalazine group; p-, phosphorylated; JAK2, Janus kinase 2; STAT3, signal transducer and activator of transcription 3; IL-6, ZO-1, zona occludens-1.
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    Image Search Results


    Naringin inhibits JAK2/STAT3 signaling and restores tight junction proteins in dextran sulfate sodium-induced colitis. (A) Representative western blotting images of p-JAK2, JAK2, p-STAT3, STAT3, IL-6, occludin, ZO-1 and β-actin expression in colon tissues. Densitometric semi-quantification of the relative protein expression levels of (B) p-JAK2/β-actin, (C) JAK2/β-actin, (D) p-JAK2/JAK2, (E) p-STAT3/β-actin, (F) STAT3/β-actin, (G) p-STAT3/STAT3, (H) IL-6/β-actin, (I) occludin/β-actin and (J) ZO-1/β-actin. Data are presented as mean ± SEM. n=3. *P<0.05 and **P<0.01 vs. control group; # P<0.05 and ## P<0.01 vs. normal group. One-way ANOVA followed by Tukey's post-hoc test was applied. N, normal group; C, control group; Nar, naringin group; Mes, mesalazine group; p-, phosphorylated; JAK2, Janus kinase 2; STAT3, signal transducer and activator of transcription 3; IL-6, ZO-1, zona occludens-1.

    Journal: Molecular Medicine Reports

    Article Title: Naringin ameliorates intestinal injury in ulcerative colitis model mice by modulating the JAK2/STAT3 signaling pathway

    doi: 10.3892/mmr.2026.13805

    Figure Lengend Snippet: Naringin inhibits JAK2/STAT3 signaling and restores tight junction proteins in dextran sulfate sodium-induced colitis. (A) Representative western blotting images of p-JAK2, JAK2, p-STAT3, STAT3, IL-6, occludin, ZO-1 and β-actin expression in colon tissues. Densitometric semi-quantification of the relative protein expression levels of (B) p-JAK2/β-actin, (C) JAK2/β-actin, (D) p-JAK2/JAK2, (E) p-STAT3/β-actin, (F) STAT3/β-actin, (G) p-STAT3/STAT3, (H) IL-6/β-actin, (I) occludin/β-actin and (J) ZO-1/β-actin. Data are presented as mean ± SEM. n=3. *P<0.05 and **P<0.01 vs. control group; # P<0.05 and ## P<0.01 vs. normal group. One-way ANOVA followed by Tukey's post-hoc test was applied. N, normal group; C, control group; Nar, naringin group; Mes, mesalazine group; p-, phosphorylated; JAK2, Janus kinase 2; STAT3, signal transducer and activator of transcription 3; IL-6, ZO-1, zona occludens-1.

    Article Snippet: Membranes were subsequently incubated separately with primary antibodies for p-JAK2 (1:1,000; cat. no. bs-2485R; BIOSS), JAK2 (1:1,000; cat. no. bs-0908R; BIOSS), p-STAT3 (1:1,000; cat. no. bs-1658R; BIOSS), STAT3 (1:1,000; cat. no. bs-55208R; BIOSS), occludin (1:1,000; cat. no. A2601; ABclonal Biotech Co., Ltd.), ZO-1 (1:1,000; cat. no. A0659; ABclonal Biotech Co., Ltd.) and β-actin (1:1,000; cat. no. ab8227; Abcam), and then with HRP-conjugated goat anti-rabbit IgG secondary antibody (1:5,000; cat. no. ab6721; Abcam).

    Techniques: Western Blot, Expressing, Control

    Naringin suppresses JAK2/STAT3 activation in IL-6-stimulated Caco-2 cells with STAT3 silencing. (A) Western blot analysis of p-JAK2, JAK2, p-STAT3, STAT3, occludin and ZO-1 in Caco-2 cells under indicated treatments. (B) Validation of STAT3 knockdown efficiency: Relative STAT3 expression in cells transfected with siSTAT3 vs. siNC. ## P<0.01 vs. siNC. Densitometric semi-quantification of relative protein expression levels of (C) p-JAK2/β-actin, (D) JAK2/β-actin, (E) p-JAK2/JAK2, (F) p-STAT3/β-actin, (G) STAT3/β-actin, (H) p-STAT3/ STAT3, (I) occludin/β-actin, (J) ZO-1/β-actin. Data are presented as mean ± SEM. n=3. *P<0.05 and **P<0.01 vs. IL-6 group; ## P<0.01 vs. normal group; Δ P<0.05 and ΔΔ P<0.01 IL-6 + Nar group vs. IL-6 + Nar + siSTAT3 group. One-way ANOVA followed by Tukey's post-hoc test was applied. N, normal group; Nar, naringin group; Mes, mesalazine group; p-, phosphorylated; JAK2, Janus kinase 2; STAT3, signal transducer and activator of transcription 3; ZO-1, zona occludens-1; si, small interfering RNA; NC, negative control.

    Journal: Molecular Medicine Reports

    Article Title: Naringin ameliorates intestinal injury in ulcerative colitis model mice by modulating the JAK2/STAT3 signaling pathway

    doi: 10.3892/mmr.2026.13805

    Figure Lengend Snippet: Naringin suppresses JAK2/STAT3 activation in IL-6-stimulated Caco-2 cells with STAT3 silencing. (A) Western blot analysis of p-JAK2, JAK2, p-STAT3, STAT3, occludin and ZO-1 in Caco-2 cells under indicated treatments. (B) Validation of STAT3 knockdown efficiency: Relative STAT3 expression in cells transfected with siSTAT3 vs. siNC. ## P<0.01 vs. siNC. Densitometric semi-quantification of relative protein expression levels of (C) p-JAK2/β-actin, (D) JAK2/β-actin, (E) p-JAK2/JAK2, (F) p-STAT3/β-actin, (G) STAT3/β-actin, (H) p-STAT3/ STAT3, (I) occludin/β-actin, (J) ZO-1/β-actin. Data are presented as mean ± SEM. n=3. *P<0.05 and **P<0.01 vs. IL-6 group; ## P<0.01 vs. normal group; Δ P<0.05 and ΔΔ P<0.01 IL-6 + Nar group vs. IL-6 + Nar + siSTAT3 group. One-way ANOVA followed by Tukey's post-hoc test was applied. N, normal group; Nar, naringin group; Mes, mesalazine group; p-, phosphorylated; JAK2, Janus kinase 2; STAT3, signal transducer and activator of transcription 3; ZO-1, zona occludens-1; si, small interfering RNA; NC, negative control.

    Article Snippet: Membranes were subsequently incubated separately with primary antibodies for p-JAK2 (1:1,000; cat. no. bs-2485R; BIOSS), JAK2 (1:1,000; cat. no. bs-0908R; BIOSS), p-STAT3 (1:1,000; cat. no. bs-1658R; BIOSS), STAT3 (1:1,000; cat. no. bs-55208R; BIOSS), occludin (1:1,000; cat. no. A2601; ABclonal Biotech Co., Ltd.), ZO-1 (1:1,000; cat. no. A0659; ABclonal Biotech Co., Ltd.) and β-actin (1:1,000; cat. no. ab8227; Abcam), and then with HRP-conjugated goat anti-rabbit IgG secondary antibody (1:5,000; cat. no. ab6721; Abcam).

    Techniques: Activation Assay, Western Blot, Biomarker Discovery, Knockdown, Expressing, Transfection, Small Interfering RNA, Negative Control

    Naringin inhibits JAK2/STAT3 signaling and restores tight junction proteins in dextran sulfate sodium-induced colitis. (A) Representative western blotting images of p-JAK2, JAK2, p-STAT3, STAT3, IL-6, occludin, ZO-1 and β-actin expression in colon tissues. Densitometric semi-quantification of the relative protein expression levels of (B) p-JAK2/β-actin, (C) JAK2/β-actin, (D) p-JAK2/JAK2, (E) p-STAT3/β-actin, (F) STAT3/β-actin, (G) p-STAT3/STAT3, (H) IL-6/β-actin, (I) occludin/β-actin and (J) ZO-1/β-actin. Data are presented as mean ± SEM. n=3. *P<0.05 and **P<0.01 vs. control group; # P<0.05 and ## P<0.01 vs. normal group. One-way ANOVA followed by Tukey's post-hoc test was applied. N, normal group; C, control group; Nar, naringin group; Mes, mesalazine group; p-, phosphorylated; JAK2, Janus kinase 2; STAT3, signal transducer and activator of transcription 3; IL-6, ZO-1, zona occludens-1.

    Journal: Molecular Medicine Reports

    Article Title: Naringin ameliorates intestinal injury in ulcerative colitis model mice by modulating the JAK2/STAT3 signaling pathway

    doi: 10.3892/mmr.2026.13805

    Figure Lengend Snippet: Naringin inhibits JAK2/STAT3 signaling and restores tight junction proteins in dextran sulfate sodium-induced colitis. (A) Representative western blotting images of p-JAK2, JAK2, p-STAT3, STAT3, IL-6, occludin, ZO-1 and β-actin expression in colon tissues. Densitometric semi-quantification of the relative protein expression levels of (B) p-JAK2/β-actin, (C) JAK2/β-actin, (D) p-JAK2/JAK2, (E) p-STAT3/β-actin, (F) STAT3/β-actin, (G) p-STAT3/STAT3, (H) IL-6/β-actin, (I) occludin/β-actin and (J) ZO-1/β-actin. Data are presented as mean ± SEM. n=3. *P<0.05 and **P<0.01 vs. control group; # P<0.05 and ## P<0.01 vs. normal group. One-way ANOVA followed by Tukey's post-hoc test was applied. N, normal group; C, control group; Nar, naringin group; Mes, mesalazine group; p-, phosphorylated; JAK2, Janus kinase 2; STAT3, signal transducer and activator of transcription 3; IL-6, ZO-1, zona occludens-1.

    Article Snippet: The membranes were blocked with 5% non-fat dry milk in Tris-buffered saline containing 0.1% Tween-20 (TBST) for 2 h at room temperature, then incubated at 4°C overnight with primary antibodies against IL-6 (1:1,000; cat. no. Bs-0782R; BIOSS), phosphorylated (p-)JAK2 (1:1,000; cat. no. bs-2485R; BIOSS), JAK2 (1:1,000; cat. no. bs-0908R; BIOSS), p-STAT3 (1:1,000; cat. no. bs-1658R; BIOSS), STAT3 (1:1,000; cat. no. bs-55208R; BIOSS), occludin (1:1,000; cat. no. A2601; ABclonal Biotech Co., Ltd.), zona occludens-1 (ZO-1; 1:1,000; cat. no. A0659; ABclonal Biotech Co., Ltd.) and β-actin (1:1,000; cat. no. ab8227; Abcam).

    Techniques: Western Blot, Expressing, Control

    Naringin suppresses JAK2/STAT3 activation in IL-6-stimulated Caco-2 cells with STAT3 silencing. (A) Western blot analysis of p-JAK2, JAK2, p-STAT3, STAT3, occludin and ZO-1 in Caco-2 cells under indicated treatments. (B) Validation of STAT3 knockdown efficiency: Relative STAT3 expression in cells transfected with siSTAT3 vs. siNC. ## P<0.01 vs. siNC. Densitometric semi-quantification of relative protein expression levels of (C) p-JAK2/β-actin, (D) JAK2/β-actin, (E) p-JAK2/JAK2, (F) p-STAT3/β-actin, (G) STAT3/β-actin, (H) p-STAT3/ STAT3, (I) occludin/β-actin, (J) ZO-1/β-actin. Data are presented as mean ± SEM. n=3. *P<0.05 and **P<0.01 vs. IL-6 group; ## P<0.01 vs. normal group; Δ P<0.05 and ΔΔ P<0.01 IL-6 + Nar group vs. IL-6 + Nar + siSTAT3 group. One-way ANOVA followed by Tukey's post-hoc test was applied. N, normal group; Nar, naringin group; Mes, mesalazine group; p-, phosphorylated; JAK2, Janus kinase 2; STAT3, signal transducer and activator of transcription 3; ZO-1, zona occludens-1; si, small interfering RNA; NC, negative control.

    Journal: Molecular Medicine Reports

    Article Title: Naringin ameliorates intestinal injury in ulcerative colitis model mice by modulating the JAK2/STAT3 signaling pathway

    doi: 10.3892/mmr.2026.13805

    Figure Lengend Snippet: Naringin suppresses JAK2/STAT3 activation in IL-6-stimulated Caco-2 cells with STAT3 silencing. (A) Western blot analysis of p-JAK2, JAK2, p-STAT3, STAT3, occludin and ZO-1 in Caco-2 cells under indicated treatments. (B) Validation of STAT3 knockdown efficiency: Relative STAT3 expression in cells transfected with siSTAT3 vs. siNC. ## P<0.01 vs. siNC. Densitometric semi-quantification of relative protein expression levels of (C) p-JAK2/β-actin, (D) JAK2/β-actin, (E) p-JAK2/JAK2, (F) p-STAT3/β-actin, (G) STAT3/β-actin, (H) p-STAT3/ STAT3, (I) occludin/β-actin, (J) ZO-1/β-actin. Data are presented as mean ± SEM. n=3. *P<0.05 and **P<0.01 vs. IL-6 group; ## P<0.01 vs. normal group; Δ P<0.05 and ΔΔ P<0.01 IL-6 + Nar group vs. IL-6 + Nar + siSTAT3 group. One-way ANOVA followed by Tukey's post-hoc test was applied. N, normal group; Nar, naringin group; Mes, mesalazine group; p-, phosphorylated; JAK2, Janus kinase 2; STAT3, signal transducer and activator of transcription 3; ZO-1, zona occludens-1; si, small interfering RNA; NC, negative control.

    Article Snippet: The membranes were blocked with 5% non-fat dry milk in Tris-buffered saline containing 0.1% Tween-20 (TBST) for 2 h at room temperature, then incubated at 4°C overnight with primary antibodies against IL-6 (1:1,000; cat. no. Bs-0782R; BIOSS), phosphorylated (p-)JAK2 (1:1,000; cat. no. bs-2485R; BIOSS), JAK2 (1:1,000; cat. no. bs-0908R; BIOSS), p-STAT3 (1:1,000; cat. no. bs-1658R; BIOSS), STAT3 (1:1,000; cat. no. bs-55208R; BIOSS), occludin (1:1,000; cat. no. A2601; ABclonal Biotech Co., Ltd.), zona occludens-1 (ZO-1; 1:1,000; cat. no. A0659; ABclonal Biotech Co., Ltd.) and β-actin (1:1,000; cat. no. ab8227; Abcam).

    Techniques: Activation Assay, Western Blot, Biomarker Discovery, Knockdown, Expressing, Transfection, Small Interfering RNA, Negative Control

    Naringin inhibits JAK2/STAT3 signaling and restores tight junction proteins in dextran sulfate sodium-induced colitis. (A) Representative western blotting images of p-JAK2, JAK2, p-STAT3, STAT3, IL-6, occludin, ZO-1 and β-actin expression in colon tissues. Densitometric semi-quantification of the relative protein expression levels of (B) p-JAK2/β-actin, (C) JAK2/β-actin, (D) p-JAK2/JAK2, (E) p-STAT3/β-actin, (F) STAT3/β-actin, (G) p-STAT3/STAT3, (H) IL-6/β-actin, (I) occludin/β-actin and (J) ZO-1/β-actin. Data are presented as mean ± SEM. n=3. *P<0.05 and **P<0.01 vs. control group; # P<0.05 and ## P<0.01 vs. normal group. One-way ANOVA followed by Tukey's post-hoc test was applied. N, normal group; C, control group; Nar, naringin group; Mes, mesalazine group; p-, phosphorylated; JAK2, Janus kinase 2; STAT3, signal transducer and activator of transcription 3; IL-6, ZO-1, zona occludens-1.

    Journal: Molecular Medicine Reports

    Article Title: Naringin ameliorates intestinal injury in ulcerative colitis model mice by modulating the JAK2/STAT3 signaling pathway

    doi: 10.3892/mmr.2026.13805

    Figure Lengend Snippet: Naringin inhibits JAK2/STAT3 signaling and restores tight junction proteins in dextran sulfate sodium-induced colitis. (A) Representative western blotting images of p-JAK2, JAK2, p-STAT3, STAT3, IL-6, occludin, ZO-1 and β-actin expression in colon tissues. Densitometric semi-quantification of the relative protein expression levels of (B) p-JAK2/β-actin, (C) JAK2/β-actin, (D) p-JAK2/JAK2, (E) p-STAT3/β-actin, (F) STAT3/β-actin, (G) p-STAT3/STAT3, (H) IL-6/β-actin, (I) occludin/β-actin and (J) ZO-1/β-actin. Data are presented as mean ± SEM. n=3. *P<0.05 and **P<0.01 vs. control group; # P<0.05 and ## P<0.01 vs. normal group. One-way ANOVA followed by Tukey's post-hoc test was applied. N, normal group; C, control group; Nar, naringin group; Mes, mesalazine group; p-, phosphorylated; JAK2, Janus kinase 2; STAT3, signal transducer and activator of transcription 3; IL-6, ZO-1, zona occludens-1.

    Article Snippet: Membranes were subsequently incubated separately with primary antibodies for p-JAK2 (1:1,000; cat. no. bs-2485R; BIOSS), JAK2 (1:1,000; cat. no. bs-0908R; BIOSS), p-STAT3 (1:1,000; cat. no. bs-1658R; BIOSS), STAT3 (1:1,000; cat. no. bs-55208R; BIOSS), occludin (1:1,000; cat. no. A2601; ABclonal Biotech Co., Ltd.), ZO-1 (1:1,000; cat. no. A0659; ABclonal Biotech Co., Ltd.) and β-actin (1:1,000; cat. no. ab8227; Abcam), and then with HRP-conjugated goat anti-rabbit IgG secondary antibody (1:5,000; cat. no. ab6721; Abcam).

    Techniques: Western Blot, Expressing, Control

    Naringin suppresses JAK2/STAT3 activation in IL-6-stimulated Caco-2 cells with STAT3 silencing. (A) Western blot analysis of p-JAK2, JAK2, p-STAT3, STAT3, occludin and ZO-1 in Caco-2 cells under indicated treatments. (B) Validation of STAT3 knockdown efficiency: Relative STAT3 expression in cells transfected with siSTAT3 vs. siNC. ## P<0.01 vs. siNC. Densitometric semi-quantification of relative protein expression levels of (C) p-JAK2/β-actin, (D) JAK2/β-actin, (E) p-JAK2/JAK2, (F) p-STAT3/β-actin, (G) STAT3/β-actin, (H) p-STAT3/ STAT3, (I) occludin/β-actin, (J) ZO-1/β-actin. Data are presented as mean ± SEM. n=3. *P<0.05 and **P<0.01 vs. IL-6 group; ## P<0.01 vs. normal group; Δ P<0.05 and ΔΔ P<0.01 IL-6 + Nar group vs. IL-6 + Nar + siSTAT3 group. One-way ANOVA followed by Tukey's post-hoc test was applied. N, normal group; Nar, naringin group; Mes, mesalazine group; p-, phosphorylated; JAK2, Janus kinase 2; STAT3, signal transducer and activator of transcription 3; ZO-1, zona occludens-1; si, small interfering RNA; NC, negative control.

    Journal: Molecular Medicine Reports

    Article Title: Naringin ameliorates intestinal injury in ulcerative colitis model mice by modulating the JAK2/STAT3 signaling pathway

    doi: 10.3892/mmr.2026.13805

    Figure Lengend Snippet: Naringin suppresses JAK2/STAT3 activation in IL-6-stimulated Caco-2 cells with STAT3 silencing. (A) Western blot analysis of p-JAK2, JAK2, p-STAT3, STAT3, occludin and ZO-1 in Caco-2 cells under indicated treatments. (B) Validation of STAT3 knockdown efficiency: Relative STAT3 expression in cells transfected with siSTAT3 vs. siNC. ## P<0.01 vs. siNC. Densitometric semi-quantification of relative protein expression levels of (C) p-JAK2/β-actin, (D) JAK2/β-actin, (E) p-JAK2/JAK2, (F) p-STAT3/β-actin, (G) STAT3/β-actin, (H) p-STAT3/ STAT3, (I) occludin/β-actin, (J) ZO-1/β-actin. Data are presented as mean ± SEM. n=3. *P<0.05 and **P<0.01 vs. IL-6 group; ## P<0.01 vs. normal group; Δ P<0.05 and ΔΔ P<0.01 IL-6 + Nar group vs. IL-6 + Nar + siSTAT3 group. One-way ANOVA followed by Tukey's post-hoc test was applied. N, normal group; Nar, naringin group; Mes, mesalazine group; p-, phosphorylated; JAK2, Janus kinase 2; STAT3, signal transducer and activator of transcription 3; ZO-1, zona occludens-1; si, small interfering RNA; NC, negative control.

    Article Snippet: Membranes were subsequently incubated separately with primary antibodies for p-JAK2 (1:1,000; cat. no. bs-2485R; BIOSS), JAK2 (1:1,000; cat. no. bs-0908R; BIOSS), p-STAT3 (1:1,000; cat. no. bs-1658R; BIOSS), STAT3 (1:1,000; cat. no. bs-55208R; BIOSS), occludin (1:1,000; cat. no. A2601; ABclonal Biotech Co., Ltd.), ZO-1 (1:1,000; cat. no. A0659; ABclonal Biotech Co., Ltd.) and β-actin (1:1,000; cat. no. ab8227; Abcam), and then with HRP-conjugated goat anti-rabbit IgG secondary antibody (1:5,000; cat. no. ab6721; Abcam).

    Techniques: Activation Assay, Western Blot, Biomarker Discovery, Knockdown, Expressing, Transfection, Small Interfering RNA, Negative Control

    ELF5 regulate casein synthesis in GMECs. (A, B) The expression of αS1-casein, αS2-casein, β-casein, κ-casein, phosphorylated JAK2 and STAT5 after transfection with pcDNA3.1-ELF5 or pcDNA3.1-NC for 48 h. (C, D) The expression of αS1-casein, αS2-casein, β-casein, κ-casein, p-JAK2, and p-STAT5 after transfection with siRNA-ELF5 or siRNA-NC (100 nM) for 48 h. The relative protein abundance of αS1-casein, αS2-casein, β-casein, and κ-casein was normalized to β-tubulin. The relative protein abundance of p-JAK2 and p-STAT5 was normalized to total JAK2 and STAT5, respectively. Values are presented as mean±SEM. * p<0.05, ** p<0.01. siRNA, small interfering ribonucleic acid; NC, negative control; GMECs, goat mammary epithelial cells; SEM, standard error of the mean.

    Journal: Animal Bioscience

    Article Title: ELF5 modulates casein synthesis in goat mammary epithelial cells via JAK2/STAT5 signaling pathway

    doi: 10.5713/ab.25.0181

    Figure Lengend Snippet: ELF5 regulate casein synthesis in GMECs. (A, B) The expression of αS1-casein, αS2-casein, β-casein, κ-casein, phosphorylated JAK2 and STAT5 after transfection with pcDNA3.1-ELF5 or pcDNA3.1-NC for 48 h. (C, D) The expression of αS1-casein, αS2-casein, β-casein, κ-casein, p-JAK2, and p-STAT5 after transfection with siRNA-ELF5 or siRNA-NC (100 nM) for 48 h. The relative protein abundance of αS1-casein, αS2-casein, β-casein, and κ-casein was normalized to β-tubulin. The relative protein abundance of p-JAK2 and p-STAT5 was normalized to total JAK2 and STAT5, respectively. Values are presented as mean±SEM. * p<0.05, ** p<0.01. siRNA, small interfering ribonucleic acid; NC, negative control; GMECs, goat mammary epithelial cells; SEM, standard error of the mean.

    Article Snippet: For the inhibition of JAK2/STAT5 pathway, JAK2 inhibitor AG490 (30 μM, MedChemExpress) or STAT5 inhibitor STAT5-IN-1 (50 μM, MedChemExpress) were treated with cells.

    Techniques: Expressing, Transfection, Quantitative Proteomics, Negative Control

    The protein abundance of caseins after JAK2 and STAT5 inhibition in GMECs. (A) The expression of αS1-casein, αS2-casein, β-casein, κ-casein, and phosphorylated JAK2 and STAT5 after JAK2 inhibitor Tyrphosting AG490 (30 μM) treatment for 48 h. (B) The expression of αS1-casein, αS2-casein, β-casein, κ-casein, and p-STAT5 after STAT5 inhibitor STAT5-IN-1 (50 μM) treatment for 48 h. The relative protein abundance of αS1-casein, αS2-casein, β-casein, and κ-casein was normalized to β-tubulin. The relative protein abundance of p-JAK2 and p-STAT5 was normalized to total JAK2 and STAT5, respectively. Values are presented as mean±SEM. ** p<0.01. GMECs, goat mammary epithelial cells; SEM, standard error of the mean.

    Journal: Animal Bioscience

    Article Title: ELF5 modulates casein synthesis in goat mammary epithelial cells via JAK2/STAT5 signaling pathway

    doi: 10.5713/ab.25.0181

    Figure Lengend Snippet: The protein abundance of caseins after JAK2 and STAT5 inhibition in GMECs. (A) The expression of αS1-casein, αS2-casein, β-casein, κ-casein, and phosphorylated JAK2 and STAT5 after JAK2 inhibitor Tyrphosting AG490 (30 μM) treatment for 48 h. (B) The expression of αS1-casein, αS2-casein, β-casein, κ-casein, and p-STAT5 after STAT5 inhibitor STAT5-IN-1 (50 μM) treatment for 48 h. The relative protein abundance of αS1-casein, αS2-casein, β-casein, and κ-casein was normalized to β-tubulin. The relative protein abundance of p-JAK2 and p-STAT5 was normalized to total JAK2 and STAT5, respectively. Values are presented as mean±SEM. ** p<0.01. GMECs, goat mammary epithelial cells; SEM, standard error of the mean.

    Article Snippet: For the inhibition of JAK2/STAT5 pathway, JAK2 inhibitor AG490 (30 μM, MedChemExpress) or STAT5 inhibitor STAT5-IN-1 (50 μM, MedChemExpress) were treated with cells.

    Techniques: Quantitative Proteomics, Inhibition, Expressing

    ELF5 mediates casein synthesis by JAK2 and STAT5 activity in GMECs. (A) Cells were treated with Tyrphosting AG490 (30 μM) or DMSO, followed by pcDNA3.1-ELF5 or pcDNA3.1-NC transfection for 48 h. (B) Cells were treated with Tyrphosting AG490 (30 μM) or DMSO, followed by siRNA-ELF5 or siRNA-NC (100 nM) transfection for 48 h. The protein abundances of αS1-casein, αS2-casein, β-casein, κ-casein, p-JAK2, and p-STAT5 were detected. The relative protein abundance of αS1-casein, αS2-casein, β-casein, and κ-casein was normalized to β-tubulin. The relative protein abundance of p-JAK2 and p-STAT5 was normalized to total JAK2 and STAT5, respectively. Values are presented as mean±SEM. a–d Different lowercase letters represent significant differences (* p<0.05). NC, negative control; siRNA, small interfering ribonucleic acid; GMECs, goat mammary epithelial cells; SEM, standard error of the mean.

    Journal: Animal Bioscience

    Article Title: ELF5 modulates casein synthesis in goat mammary epithelial cells via JAK2/STAT5 signaling pathway

    doi: 10.5713/ab.25.0181

    Figure Lengend Snippet: ELF5 mediates casein synthesis by JAK2 and STAT5 activity in GMECs. (A) Cells were treated with Tyrphosting AG490 (30 μM) or DMSO, followed by pcDNA3.1-ELF5 or pcDNA3.1-NC transfection for 48 h. (B) Cells were treated with Tyrphosting AG490 (30 μM) or DMSO, followed by siRNA-ELF5 or siRNA-NC (100 nM) transfection for 48 h. The protein abundances of αS1-casein, αS2-casein, β-casein, κ-casein, p-JAK2, and p-STAT5 were detected. The relative protein abundance of αS1-casein, αS2-casein, β-casein, and κ-casein was normalized to β-tubulin. The relative protein abundance of p-JAK2 and p-STAT5 was normalized to total JAK2 and STAT5, respectively. Values are presented as mean±SEM. a–d Different lowercase letters represent significant differences (* p<0.05). NC, negative control; siRNA, small interfering ribonucleic acid; GMECs, goat mammary epithelial cells; SEM, standard error of the mean.

    Article Snippet: For the inhibition of JAK2/STAT5 pathway, JAK2 inhibitor AG490 (30 μM, MedChemExpress) or STAT5 inhibitor STAT5-IN-1 (50 μM, MedChemExpress) were treated with cells.

    Techniques: Activity Assay, Transfection, Quantitative Proteomics, Negative Control

    Molecular mechanism of ELF5 promotes casein synthesis by enhancing the activity of JAK2/STAT5 signaling pathway in goat mammary epithelial cells. PRLR stands for prolactin receptor.

    Journal: Animal Bioscience

    Article Title: ELF5 modulates casein synthesis in goat mammary epithelial cells via JAK2/STAT5 signaling pathway

    doi: 10.5713/ab.25.0181

    Figure Lengend Snippet: Molecular mechanism of ELF5 promotes casein synthesis by enhancing the activity of JAK2/STAT5 signaling pathway in goat mammary epithelial cells. PRLR stands for prolactin receptor.

    Article Snippet: For the inhibition of JAK2/STAT5 pathway, JAK2 inhibitor AG490 (30 μM, MedChemExpress) or STAT5 inhibitor STAT5-IN-1 (50 μM, MedChemExpress) were treated with cells.

    Techniques: Activity Assay

    Fatty acid‐binding protein (A‐FABP) mediates neuroinflammation via the JAK2/STAT3 signalling pathway. (A) Workflow diagram. Proteomic analysis of brain tissue around the subarachnoid space from the subarachnoid haemorrhage (SAH)‐treated Veh group and the SAH‐treated BMS group ( n = 4). (B) KEGG enrichment highlights the JAK‐STAT signalling pathway. (C) Volcano plot demonstrates the results of 85 differentially expressed proteins. STAT3 is labelled in green. (D–H) Representative western blot images and quantitative analyses of (E) p‐STAT3/STAT3, (F) p‐JAK1/JAK1, (G) p‐JAK2/JAK2 and (H) p‐JAK3/JAK3 in WT and knockout (KO) mice after SAH. (I–L) Representative western blot images and quantitative analyses of (J) TNF‐α, (K) IL‐1β and (L) IL‐6 in different groups. (M and N) Representative images and quantitative analysis of TUNEL staining with co‐staining with NeuN (red) and TUNEL‐positive neurons (green, scale bar = 100 µm, n = 6). Data are presented as means ± SD. * p < .05, ** p < .01, *** p < .001. C‐A1, coumermycin A1; ns, no significance. Source : Schematic diagram created with BioRender.com.

    Journal: Clinical and Translational Medicine

    Article Title: Adipocyte fatty acid‐binding protein as a cerebrospinal fluid–accessible biomarker and druggable target in subarachnoid haemorrhage: Linking fatty acid dysregulation to microglial neuroinflammation

    doi: 10.1002/ctm2.70607

    Figure Lengend Snippet: Fatty acid‐binding protein (A‐FABP) mediates neuroinflammation via the JAK2/STAT3 signalling pathway. (A) Workflow diagram. Proteomic analysis of brain tissue around the subarachnoid space from the subarachnoid haemorrhage (SAH)‐treated Veh group and the SAH‐treated BMS group ( n = 4). (B) KEGG enrichment highlights the JAK‐STAT signalling pathway. (C) Volcano plot demonstrates the results of 85 differentially expressed proteins. STAT3 is labelled in green. (D–H) Representative western blot images and quantitative analyses of (E) p‐STAT3/STAT3, (F) p‐JAK1/JAK1, (G) p‐JAK2/JAK2 and (H) p‐JAK3/JAK3 in WT and knockout (KO) mice after SAH. (I–L) Representative western blot images and quantitative analyses of (J) TNF‐α, (K) IL‐1β and (L) IL‐6 in different groups. (M and N) Representative images and quantitative analysis of TUNEL staining with co‐staining with NeuN (red) and TUNEL‐positive neurons (green, scale bar = 100 µm, n = 6). Data are presented as means ± SD. * p < .05, ** p < .01, *** p < .001. C‐A1, coumermycin A1; ns, no significance. Source : Schematic diagram created with BioRender.com.

    Article Snippet: JAK2 activator coumermycin A1 (C‐A1, #HY‐N7452, 100 μg/kg; MCE, USA) was administered intraperitoneally for 1 h after SAH.

    Techniques: Binding Assay, Western Blot, Knock-Out, TUNEL Assay, Staining