antibodies against il 6  (Bioss)

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 restores barrier function in IL-6-induced Caco-2 cells. (A) Transepithelial electrical resistance values over time. (B) Fluorescein isothiocyanate-dextran 4 kDa permeability assay. n=6. Data are presented as mean ± SEM. **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. Nar, naringin.

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: Permeability

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: Frontiers in Nutrition

Article Title: Manifold hepatoprotective actions of α-lipoic acid on metabolic function through redox regulation, inflammatory modulation, and anti-apoptosis after chronic sleep-deprived injury

doi: 10.3389/fnut.2025.1679494

Figure Lengend Snippet: Photomicrographs (A–I) , immunoblot (J) , and histogram (K) showed the expression of key inflammatory factors in the liver of control (CSC), chronic sleep deprivation (CSD), and chronic sleep deprivation with alpha lipoic acid treatment (CSD + ALA) rats. Note that the expressions of all the detected inflammatory factors (such as NF-κB, TNF-α, IL-6, IL-1β, and COX2) were remarkably increased in the liver following CSD as demonstrated by both immunohistochemical staining (B,E,H) and Western blotting (J) . Also note that in rats subjected to CSD and received ALA treatment, the expression of all above inflammatory factors were significantly decreased to near the levels of the control ones (C,F,I,J,K) . These results clearly indicate that CSD would considerably induce hepatic inflammation, which could successfully be depressed by ALA treatment. * p < 0.05 compared to control value; # p < 0.05 compared to CSD group. CV: Central Vein. Scale bar = 100 μm.

Article Snippet: Subsequently, the sections were reacted with the following primary antibodies: NF-κB (p65) (1:200, Santa Cruz, sc-8008), IL-6 (1:500, Bioss bs-0782R-TR), COX2 (1:200, Santa Cruz, sc-376861), BAX (1:100, Santa Cruz, sc-7480), Bcl-2 (1:200, Millipore, AB1722), GPx4 (1:100, Abcam, ab125066), and FACL4 (1:200, Abcam, ab155282) in blocking medium for 48 h at 4 °C.

Techniques: Western Blot, Expressing, Control, Immunohistochemical staining, Staining