Journal: International Journal of Molecular Medicine

Article Title: Triptolide exerts antiviral effects and alleviates influenza A-induced pneumonia by inhibiting the overactivation of absent in melanoma 2 signaling in immune cells

doi: 10.3892/ijmm.2026.5829

Figure Lengend Snippet: H1N1 infection affects cell viability, inflammatory cytokine secretion and interactions between HBEpiCs and THP-1 cells. (A) CCK-8 assay revealed that HBEpiC viability decreased in a concentration-dependent manner following H1N1 infection. (B) ELISA revealed that the levels of IL-1β, IL-6, TNF-α, and IL-8 in HBEpiCs decreased with increasing H1N1 infection. (C) CCK-8 assay indicated that supernatants from H1N1-infected HBEpiC cultures reduced the viability of THP-1 cells in a dose-dependent manner. (D) ELISA results suggested that the levels of inflammatory cytokines (IL-1β, IL-6, TNF-α and IL-8) in THP-1 cells were decreased following exposure to supernatants from H1N1-infected HBEpiC cultures. (E) Cell adhesion assay revealed that the number of THP-1 cells adhering to HBEpiCs increased with increasing H1N1 concentration (scale bar, 10 μ m). Arrow indicates THP-1 cells that remain attached to the surface of HBEpiCs, highlighting the adhesion interaction between the two cell types. (F) Transwell assay suggested that H1N1 infection enhanced the migration capacity of THP-1 cells, with increased migration observed at higher virus concentrations (scale bar, 50 μ m). The data are presented as the mean ± standard deviation; ** P<0.01, *** P<0.001 vs. control. H1N1, influenza A; HBEpiCs, human bronchial epithelial cells; ELISA, enzyme-linked immunosorbent assay; IL, interleukin; TNF-α, tumor necrosis factor-α; Con, control; MOI, multiplicity of infection.

Article Snippet: Cell supernatants were collected and analyzed using Human TNF-α High Sensitivity ELISA Kit [cat. no. EK182HS; Hangzhou Multi Sciences (Lianke) Biotech Co., Ltd.], Human IL-8 ELISA Kit [cat. no. EK108; Hangzhou Multi Sciences (Lianke) Biotech Co., Ltd.], a human IL-1β ELISA kit [EH0185; Hangzhou Multi Sciences (Lianke) Biotech Co., Ltd.] and IL-6 [cat. no. EK1217; Hangzhou Multi Sciences (Lianke) Biotech Co., Ltd.] according to the manufacturer's instructions.

Techniques: Infection, CCK-8 Assay, Concentration Assay, Enzyme-linked Immunosorbent Assay, Cell Adhesion Assay, Transwell Assay, Migration, Virus, Standard Deviation, Control

Journal: International Journal of Molecular Medicine

Article Title: Triptolide exerts antiviral effects and alleviates influenza A-induced pneumonia by inhibiting the overactivation of absent in melanoma 2 signaling in immune cells

doi: 10.3892/ijmm.2026.5829

Figure Lengend Snippet: TP modulates the inflammatory response and immune cell activity in H1N1-infected HBEpiCs and THP-1 cells. (A) No significant changes were observed in HBEpiCs treated with various concentrations of TP (5, 10 and 20 nM) following H1N1 infection compared with the control. (B) After TP treatment, the levels of the inflammatory cytokines IL-1β, IL-6, TNF-α and IL-8 in HBEpiCs were markedly lower than those in the untreated group. (C) The viability of THP-1 cells pretreated with H1N1-infected HBEpiC culture supernatant decreased after TP treatment. (D) The levels of IL-1β, IL-6, TNF-α, and IL-8 in THP-1 cells were markedly lower after TP treatment. (E) The adhesion of THP-1 cells to HBEpiCs induced by H1N1 infection decreased in a dose-dependent manner with increasing TP concentration (scale bar, 10 μ m). Arrow indicates THP-1 cells that remain attached to the surface of HBEpiCs, highlighting the adhesion interaction between the two cell types. (F) The migration capacity of THP-1 cells was markedly reduced when the supernatant from H1N1-infected HBEpiC cultures was treated with TP (scale bar, 50 μ m). The data are presented as the mean ± standard deviation; * P<0.05, ** P<0.01, *** P<0.001 vs. control. TP, triptolide; H1N1, influenza A; HBEpiCs, human bronchial epithelial cells; IL, interleukin; TNF-α, tumor necrosis factor-α; Con, control.

Article Snippet: Cell supernatants were collected and analyzed using Human TNF-α High Sensitivity ELISA Kit [cat. no. EK182HS; Hangzhou Multi Sciences (Lianke) Biotech Co., Ltd.], Human IL-8 ELISA Kit [cat. no. EK108; Hangzhou Multi Sciences (Lianke) Biotech Co., Ltd.], a human IL-1β ELISA kit [EH0185; Hangzhou Multi Sciences (Lianke) Biotech Co., Ltd.] and IL-6 [cat. no. EK1217; Hangzhou Multi Sciences (Lianke) Biotech Co., Ltd.] according to the manufacturer's instructions.

Techniques: Activity Assay, Infection, Control, Concentration Assay, Migration, Standard Deviation

Journal: Bioactive Materials

Article Title: Energetic metabolism-regulatory glycopeptide hydrogel accelerates pressure ulcer wound repair

doi: 10.1016/j.bioactmat.2026.02.016

Figure Lengend Snippet: GMI gel -mediated metabolic reprogramming and its regulatory role in macrophage polarization. A-D) Hexokinase activity, Phosphofructokinase activity, Isocitrate dehydrogenase activity, and Succinate dehydrogenase activity, n = 3. E-H) Heatmap of LC-MS data and quantitative analysis of the relative abundance of glycolysis and TCA cycle metabolites, n = 3. I) Schematic diagram of glycolysis and the TCA cycle. J) Representative CLSM images of RAW 264.7 cells treated with GMI gel for 72 h. K) Flow cytometry analysis of CD206 and CD86 expression. L, M) The secretion of IL-6 and TNF-α in the culture supernatant of RAW264.7 cells, n = 3. Data are shown as mean ± SDs. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, ns, not significant (p > 0.05).

Article Snippet: The expression levels of IL-6 and TNF-α in the culture medium were measured using commercial ELISA kits (Cusabio, Wuhan, China).

Techniques: Activity Assay, Liquid Chromatography with Mass Spectroscopy, Flow Cytometry, Expressing

Journal: Bioactive Materials

Article Title: Energetic metabolism-regulatory glycopeptide hydrogel accelerates pressure ulcer wound repair

doi: 10.1016/j.bioactmat.2026.02.016

Figure Lengend Snippet: GMI gel promotes the healing of infected pressure ulcers in vivo. A) Schematic diagram of GMI gel treatment of infected pressure ulcers. B) Photographs of wounds in mice at different treatment times. C) Signs of wound closure. D) Wound size at different treatment times, n = 3. E) H&E staining images of mouse wound tissue after different treatments on day 12. F) Masson staining images of mouse wound tissue after different treatments on day 12. G) Representative laser Doppler perfusion images of wounds in mice in each treatment group on day 12. H) Representative images of immunohistochemical staining for TNF- α, IL-6 and IL-10 12 days after treatment. I-L) Quantitative statistics of wound site blood perfusion, TNF- α, IL-6 and IL-10, n = 3. Data are shown as mean ± SDs. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Article Snippet: The expression levels of IL-6 and TNF-α in the culture medium were measured using commercial ELISA kits (Cusabio, Wuhan, China).

Techniques: Infection, In Vivo, Staining, Immunohistochemical staining

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