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

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 reverses IL-6-induced ZO-1 and occludin impairment in a STAT3-dependent manner. (A) Immunofluorescence staining for ZO-1 (blue) and occludin (green); nuclei were stained with DAPI (cyan). Merged shows the merged images of DAPI and respective protein staining. Quantitative analysis of relative (B) ZO-1 and (C) occludin protein expression. (n=3). Data are presented as mean ± SEM. *P<0.05 and **P<0.01 vs. IL-6 group; ## P<0.01 vs. normal group. One-way ANOVA followed by Tukey's post-hoc test was applied. ZO-1, zona occludens-1; N, normal group; Nar, naringin; STAT3, signal transducer and activator of transcription 3; 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: Immunofluorescence, Staining, Expressing, Small Interfering RNA, 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

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

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 reverses IL-6-induced ZO-1 and occludin impairment in a STAT3-dependent manner. (A) Immunofluorescence staining for ZO-1 (blue) and occludin (green); nuclei were stained with DAPI (cyan). Merged shows the merged images of DAPI and respective protein staining. Quantitative analysis of relative (B) ZO-1 and (C) occludin protein expression. (n=3). Data are presented as mean ± SEM. *P<0.05 and **P<0.01 vs. IL-6 group; ## P<0.01 vs. normal group. One-way ANOVA followed by Tukey's post-hoc test was applied. ZO-1, zona occludens-1; N, normal group; Nar, naringin; STAT3, signal transducer and activator of transcription 3; 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: Immunofluorescence, Staining, Expressing, Small Interfering RNA, 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

Journal: Frontiers in Immunology

Article Title: DOT1L promotes immune evasion in lung adenocarcinoma through H3K79me2-mediated epigenetic activation of immune checkpoints

doi: 10.3389/fimmu.2026.1719299

Figure Lengend Snippet: DOT1L-mediated H3K79me2 regulates immune evasion-related gene expression. (A-D) ChIP-seq profiles showing H3K79me2 enrichment in the gene regions of JAK1, STAT3, STAT1, and RELA in A549 cells. (E-G) Western blot analysis detected DOT1L and H3K79me2 protein levels after treatment with the DOT1L inhibitor SGC0946. GAPDH served as a loading control. (H-J) qPCR validation of STAT3, JAK1, and RELA mRNA downregulation upon SGC0946 treatment in three independent cell lines (* P < 0.05, ** P < 0.01 versus control.).

Article Snippet: To rescue STAT3 activity, cells were co-treated with 2 nM STAT3 agonist ML115 (MedChemExpress, HY-111152) for 48 hours.

Techniques: Gene Expression, ChIP-sequencing, Western Blot, Control, Biomarker Discovery

Journal: Frontiers in Immunology

Article Title: DOT1L promotes immune evasion in lung adenocarcinoma through H3K79me2-mediated epigenetic activation of immune checkpoints

doi: 10.3389/fimmu.2026.1719299

Figure Lengend Snippet: DOT1L promotes immune evasion in LUAD by activating the JAK1/STAT3/PD-L1 axis and inducing T-cell exhaustion. (A-C) Western blot analysis detected protein expression of DOT1L, JAK1, STAT3, p-STAT3 and PD-L1 in A549 and H1975 cells. (D) Flow cytometry analysis of PD-1+ T cell subsets in the co-cultured system of PBMCs with A549 cells(* P < 0.05 versus control).

Article Snippet: To rescue STAT3 activity, cells were co-treated with 2 nM STAT3 agonist ML115 (MedChemExpress, HY-111152) for 48 hours.

Techniques: Western Blot, Expressing, Flow Cytometry, Cell Culture, Control

Journal: Frontiers in Immunology

Article Title: DOT1L promotes immune evasion in lung adenocarcinoma through H3K79me2-mediated epigenetic activation of immune checkpoints

doi: 10.3389/fimmu.2026.1719299

Figure Lengend Snippet: Pharmacological inhibition of DOT1L exhibits antitumor effects in a LUAD tail vein lung metastasis model. (A) Bioluminescence imaging shows in vivo evaluation of PD-1 inhibitor (200 μg i.p, twice weekly), SGC0946-L group(20 mg/kg), SGC0946-H group(40 mg/kg), in the tail-vein lung metastasis model. (B) Average weight of mice in in each group, control group(blue line), PD-1 inhibitor group(green line), SGC0946-L group(purple line), SGC0946-H group(Red line). (C) Survival estimates of mice in each group. (D-G) IHC staining of DOT1L, H3K79me2, STAT3 protein expression in tumor tissues in each group. Red scale bar: 20 µm. SGC0946-L, low does group, SGC0946-H, high does group. * P < 0.05.

Article Snippet: To rescue STAT3 activity, cells were co-treated with 2 nM STAT3 agonist ML115 (MedChemExpress, HY-111152) for 48 hours.

Techniques: Inhibition, Imaging, In Vivo, Control, Immunohistochemistry, Expressing

Journal: Frontiers in Immunology

Article Title: DOT1L promotes immune evasion in lung adenocarcinoma through H3K79me2-mediated epigenetic activation of immune checkpoints

doi: 10.3389/fimmu.2026.1719299

Figure Lengend Snippet: Clinical association of DOT1L expression with metastatic progression and immune checkpoint regulation in LUAD. (A, B) IHC analysis of DOT1L and associated markers (H3K79me2, STAT3, PD-L1, PD-1, CD276, and LAG3) in LUAD tissues stratified by DOT1L expression levels. (C) Comparison of DOT1L expression between tumor and adjacent normal tissues. (D) DOT1L expression in stage IV metastatic LUAD compared to non-metastatic cases. (E-J) Pearson correlation analysis between DOT1L and immune checkpoint/epigenetic markers. (K) Pearson correlation analysis between DOT1L expression and TMB.

Article Snippet: To rescue STAT3 activity, cells were co-treated with 2 nM STAT3 agonist ML115 (MedChemExpress, HY-111152) for 48 hours.

Techniques: Expressing, Comparison