il 13  (R&D Systems)

Journal: Redox Biology

Article Title: Nrf2 pathway mediates copper oxide nanoparticle-induced exacerbation of allergic asthma

doi: 10.1016/j.redox.2026.104180

Figure Lengend Snippet: Effects of CuONPs on allergic inflammation and oxidative stress in OVA-induced asthmatic mice. (A) Airway hyperresponsiveness assessed as total respiratory system resistance in response to methacholine challenge (10, 20, and 40 mg/mL). (B–F) Total and differential inflammatory cell counts in BALF. (G–L) IL-1β, IL-6, TNF-α, IL-4, IL-5, and IL-13 levels in BALF, measured by ELISA. (M and N) Total IgE and OVA specific IgE levels in serum. (O and P) MDA levels and SOD activity in lung tissue. Data are presented as means ± SD (n = 6 mice/group). ∗∗ p < 0.01 and ∗∗∗ p < 0.001 versus NC group. # p < 0.05, ## p < 0.01, and ### p < 0.001 versus OVA group.

Article Snippet: BALF was centrifuged at 300× g for 10 min at 4 °C, and the supernatant was stored for cytokine analysis using commercially available enzyme-linked immunosorbent assay (ELISA) kits to quantify IL-1β, IL-6, tumor necrosis factor (TNF)-α, IL-4, IL-5, and IL-13 (R&D Systems, Minneapolis, MN, USA; Cat. No. MLB00C, M6000B, MTA00B, M4000B, M5000, and M1300CB, respectively).

Techniques: Enzyme-linked Immunosorbent Assay, Activity Assay

Journal: Redox Biology

Article Title: Nrf2 pathway mediates copper oxide nanoparticle-induced exacerbation of allergic asthma

doi: 10.1016/j.redox.2026.104180

Figure Lengend Snippet: Effects of Nrf2 overexpression on allergic inflammation and oxidative stress in CuONP-exposed asthmatic mice. (A) Immunofluorescence analysis of lung tissue from mice administered PBS or AAV2/8-GFP via intratracheal instillation. (B) Airway hyperresponsiveness assessed as total respiratory system resistance in response to methacholine challenge (10, 20, and 40 mg/mL). (C–G) Total and differential inflammatory cell counts in BALF. (H–M) IL-1β, IL-6, TNF-α, IL-4, IL-5, and IL-13 levels in BALF, measured by ELISA. (N and O) Total IgE and OVA specific IgE levels in serum. (P and Q) MDA levels and SOD activity in lung tissue. Data are presented as means ± SD (n = 3 mice/group for panels A; n = 6 mice/group for panels B–Q). In panel B, ## p < 0.01 indicates significant differences between GFP-NC and GFP-OVA, and ∗∗ p < 0.01 indicates significant differences between GFP-OVA + CuONPs and Nrf2-OVA + CuONPs. For panels C–Q, ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 indicate significant differences between AAV-GFP and AAV-Nrf2 within each condition.

Article Snippet: BALF was centrifuged at 300× g for 10 min at 4 °C, and the supernatant was stored for cytokine analysis using commercially available enzyme-linked immunosorbent assay (ELISA) kits to quantify IL-1β, IL-6, tumor necrosis factor (TNF)-α, IL-4, IL-5, and IL-13 (R&D Systems, Minneapolis, MN, USA; Cat. No. MLB00C, M6000B, MTA00B, M4000B, M5000, and M1300CB, respectively).

Techniques: Over Expression, Immunofluorescence, Enzyme-linked Immunosorbent Assay, Activity Assay

Journal: Redox Biology

Article Title: Hepatic supersulfides attenuate acetaminophen-induced liver injury via enhanced detoxification and anti-inflammatory mechanisms

doi: 10.1016/j.redox.2026.104140

Figure Lengend Snippet: Suppression of proinflammatory cytokine production and M1-type macrophage polarization by a supersulfide donor in livers from APAP-treated mice. (A–C) Levels of IL-1β, IL-6, and IL-10 in liver tissue. Mice were intraperitoneally administered APAP (330 mg/kg), followed by subcutaneous NAC-S2 administration at 30 min and 2 h post-APAP. Livers were harvested 24 h after APAP administration, and cytokine levels were quantified by ELISA. (D) Western blot analysis of hepatic iNOS and Arg-1 expression. (E, F) Quantification of Western blot band intensities. Relative protein levels were normalized to β-actin. Uncropped blots are shown in . Statistical analysis was performed using one-way ANOVA followed by Tukey's post hoc multiple comparisons test. Data were expressed as means ± SD (n ≥ 3). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001; # P < 0.05, # # P < 0.01, # # # P < 0.001 compared to control group.

Article Snippet: Mouse IL-1β/IL-1F2 Quantikine ELISA Kit (MLB00C), Mouse IL-6 Quantikine ELISA Kit (M6000B-1), and Mouse IL-10 Quantikine ELISA Kit (M1000B) were obtained from R&D Systems (Minneapolis, MB, USA).

Techniques: Enzyme-linked Immunosorbent Assay, Western Blot, Expressing, Control

Journal: Redox Biology

Article Title: Hepatic supersulfides attenuate acetaminophen-induced liver injury via enhanced detoxification and anti-inflammatory mechanisms

doi: 10.1016/j.redox.2026.104140

Figure Lengend Snippet: Effects of NAC-S2, oxNAC, and NAC on APAP-induced liver injury. (A) Experimental protocol. Mice were intraperitoneally administered APAP (330 mg/kg), followed by subcutaneous administration of sulfur compounds (NAC-S2, oxNAC, or NAC) at 30 min and 2 h post-APAP. Blood was collected at 8, 12, and 24 h post-APAP, and liver tissue was harvested at 24 h post-APAP. (B, C) Time-course of serum ALT and AST levels. (D) Quantification of necrotic area in liver. Macroscopic appearance and H&E staining of liver tissues are shown in Hepatic cytokine levels: IL-1β (E), IL-6 (F), and IL-10 (G). (H) Western blot analysis of iNOS and Arg-1 expression in liver. (I, J) Quantification of Western blot band intensities. Relative protein levels were normalized to β-actin. Uncropped blots are shown in . Statistical analysis was performed using one-way ANOVA followed by Tukey's post hoc multiple comparisons test. Data were expressed as means ± SD (n ≥ 3). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001; # P < 0.05, # # P < 0.01, # # # P < 0.001 compared to control group.

Article Snippet: Mouse IL-1β/IL-1F2 Quantikine ELISA Kit (MLB00C), Mouse IL-6 Quantikine ELISA Kit (M6000B-1), and Mouse IL-10 Quantikine ELISA Kit (M1000B) were obtained from R&D Systems (Minneapolis, MB, USA).

Techniques: Staining, Western Blot, Expressing, Control

Journal: Redox Biology

Article Title: Hepatic supersulfides attenuate acetaminophen-induced liver injury via enhanced detoxification and anti-inflammatory mechanisms

doi: 10.1016/j.redox.2026.104140

Figure Lengend Snippet: Effects of the supersulfide donor TGS4 on APAP-induced liver injury. (A) Experimental protocol. Mice were intraperitoneally administered APAP (330 mg/kg), followed by subcutaneous injection of TGS4 at 30 min and 2 h post-APAP. Two different doses were used as indicated. Blood was collected at 8, 12, and 24 h post-APAP, and liver tissue was harvested at 24 h post-APAP. (B, C) Time-course of serum ALT and AST levels. (D–F) Hepatic cytokine levels: IL-1β (D), IL-6 (E), and IL-10 (F). Statistical analysis was performed using one-way ANOVA followed by Tukey's post hoc multiple comparisons test. Data were expressed as means ± SD (n ≥ 4). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001; # P < 0.05, # # P < 0.01, # # # P < 0.001 compared to control group.

Article Snippet: Mouse IL-1β/IL-1F2 Quantikine ELISA Kit (MLB00C), Mouse IL-6 Quantikine ELISA Kit (M6000B-1), and Mouse IL-10 Quantikine ELISA Kit (M1000B) were obtained from R&D Systems (Minneapolis, MB, USA).

Techniques: Injection, Control

Journal: iScience

Article Title: Serglycin modulates inflammation and metabolism in macrophages

doi: 10.1016/j.isci.2026.115235

Figure Lengend Snippet: SRGN deficiency reshapes the inflammatory secretome and transcriptional programs in human macrophages (A) Volcano plot of differentially secreted proteins between SRGN −/− and wild-type THP-1 macrophages under M1 polarization. Among 1,507 quantified proteins, 53 were significantly altered (adjusted p < 0.05), with serglycin being the most downregulated protein in knockout cells. (B) Validation of selected targets by RT-qPCR. SRGN −/− M1 macrophages showed significantly increased expression of IL6 and TNF and reduced expression of CCL5 compared with wild-type cells (mean ± SEM; unpaired Student’s t test; p < 0.05, ∗ p < 0.01, and ∗∗∗ p < 0.0001; n = 4). (C) ELISA quantification of secreted cytokines in culture supernatants. SRGN −/− macrophages secreted significantly less TNF-α, CCL5, and IL-6 compared with wild-type macrophages ( n = 4), consistent with proteomics and RNA-seq data. (D) Transmission electron microscopy (TEM) images of THP-1 M0 and M1 macrophages. Scale bars, 5 μm. Vesicles were manually annotated and quantified in 10 cells per experimental group. The number of vesicles per cell and the percentage of cellular area occupied by vesicles were significantly reduced in both M0 and M1 SRGN −/− macrophages compared with wild-type macrophages. (E) Phagocytosis assay using fluorescently labeled bioparticles. SRGN −/− macrophages exhibited reduced phagocytic capacity under both M0 and M1 conditions (mean ± SEM; unpaired Student’s t test; p < 0.05 and ∗∗ p < 0.001; n = 6).

Article Snippet: BMDMs: cytokine levels (IL6, IL-1β, IL-12p40, TGF-β1, and TNF-α) were measured in supernatants from differentiated BMDMs using ELISA kits (R&D Systems: IL6 [Cat. No. M6000B-1], IL-1β (Cat. No. MLB00C), IL-12p40 (Cat. No. M1270), TGF-β1 (Cat. No. DY1679-05, Cat. No. DY007B), TNF-α (Cat. No. MTA00B) following the manufacturer’s protocols.

Techniques: Knock-Out, Biomarker Discovery, Quantitative RT-PCR, Expressing, Enzyme-linked Immunosorbent Assay, RNA Sequencing, Transmission Assay, Electron Microscopy, Phagocytosis Assay, Labeling