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

Journal: Materials Today Bio

Article Title: Prodrug-integrated multifunctional liposome encapsulation enhances probiotic-based bacteriotherapy for inflammatory bowel disease

doi: 10.1016/j.mtbio.2026.103110

Figure Lengend Snippet: Preventative efficacy of DTI@EcN against DSS-induced colitis. ( A ) Schematic of the experimental schedule. Mice received daily oral gavage of various bacterial formulations or drugs throughout the experimental period (bacteria: 5 × 10 8 CFU; IDE: 65 mg/kg). 3% DSS was given via drinking water from day 4 to day 8 to induce colitis. ( B ) Quantitative assessment of body weight variation in colitis mice across treatment groups. ( C ) Macroscopic appearance of colon tissues and ( D ) corresponding length measurements. ( E ) Histopathological evaluation by H&E staining and ( F ) histopathological scores of colon tissues based on H&E images. Scale bar: 100 μm. ( G ) Immunofluorescence localization of tight junction proteins ZO-1 (red) and Occludin (green) in colonic epithelia. Cell nuclei were stained with DAPI (blue). Scale bar: 100 μm. ( H ) Quantified ZO-1 and ( I ) occludin fluorescence intensities in colon tissues shown in (G) through ImageJ. ( J ) LSCM images showing DCF fluorescence in colon tissues incubated with DCFH-DA, representing the relative ROS levels across different treatment groups. Scale bar: 100 μm. ( K ) Quantified DCF fluorescence intensities from (J), analyzed with ImageJ. ( L ) Relative colonic MPO activities in colon tissues in different treatment groups. ( M - P ) Levels of pro-inflammatory cytokines, including IL-6 ( M ), IL-1β ( N ), TNF-α (O), and IFN-γ ( P ), in colon tissues, determined by ELISA kits. Data represent the mean ± SEM (n = 5). Statistical analysis was performed using one-way ANOVA. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

Article Snippet: The selected chemicals and biological materials used in this research are as follows: 1-(3-dimethylaminopropyl)-3-ethylcarbodiimide (EDCI, Macklin), 4-bromobutyric acid (Bidepharm), thiourea (Macklin), sodium hydroxide (NaOH, Macklin), hydrochloric acid (HCl, Macklin), trifluoroacetic acid (Bidepharm), idebenone (Bidepharm), hexadecyltrimethylammonium bromide (Macklin), 4-dimethylaminopyridine (DMAP, Macklin), N-hydroxysuccinimide (NHS, Macklin), 2′,7′-dichlorofluorescin diacetate (DCFH-DA, Aladdin), DSPE-PEG2000-NH 2 (Yusi), DSPE-PEG2000-FITC (Yusi), cholesterol (Yuanye), trypsin (Macklin), pepsin powder (Bidepharm), bile salts (Macklin), ampicillin (Bidepharm), lysin (Bidepharm), dextran sulfate sodium salt (DSS, MW 40,000, MP Bio), LB nutrient agar (Hopebiol), Cell Counting Kit-8 (CCK-8, Beyotime), mouse IL-6, IFN-γ, IL-1β, and TNF-α uncoated ELISA kits (Thermo Fisher Scientific), and antigen retrieval solution (Servicebio).

Techniques: Bacteria, Staining, Immunofluorescence, Fluorescence, Incubation, Enzyme-linked Immunosorbent Assay

Journal: Materials Today Bio

Article Title: Prodrug-integrated multifunctional liposome encapsulation enhances probiotic-based bacteriotherapy for inflammatory bowel disease

doi: 10.1016/j.mtbio.2026.103110

Figure Lengend Snippet: Therapeutic efficacy of DTI@EcN against DSS-induced colitis. ( A ) Schematic of the experimental schedule. Colitis was induced by administering 3% DSS in drinking water for the first 5 days. Subsequently, different treatments were administered daily for 5 days to evaluate their therapeutic efficacy. ( B ) Body weight dynamics of colitis mice under different treatments. ( C ) Macroscopic colon appearance and ( D ) corresponding length measurements across groups. ( E) Histopathological assessment by H&E staining. Scale bar: 100 μm. ( F ) Histopathology scores of colon tissues based on the H&E images. ( G ) Localization of tight junction proteins ZO-1 (red) and occludin (green) in colonic epithelium across treatment groups. Cell nuclei were stained with DAPI (blue). Scale bar: 100 μm. ( H ) Quantification of ZO-1 and ( I ) Occludin fluorescence intensities from (G), analyzed using ImageJ. ( J ) LSCM images showing DCF fluorescence in colon tissues incubated with DCFH-DA, representing the relative ROS levels across different treatment groups. Scale bar: 100 μm. ( K ) Quantitative analysis of DCF fluorescence intensities from (J). ( L ) Relative MPO activity in colon tissues across various treatment groups. ( M - P ) Levels of pro-inflammatory cytokines, including IL-6 ( M ), IL-1β ( N ), TNF-α ( O ), and IFN-γ ( P ), in colon tissues, measured by ELISA kits. Data represented the mean ± SEM (n = 5 or 6). Statistical analysis was performed using one-way ANOVA. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

Article Snippet: The selected chemicals and biological materials used in this research are as follows: 1-(3-dimethylaminopropyl)-3-ethylcarbodiimide (EDCI, Macklin), 4-bromobutyric acid (Bidepharm), thiourea (Macklin), sodium hydroxide (NaOH, Macklin), hydrochloric acid (HCl, Macklin), trifluoroacetic acid (Bidepharm), idebenone (Bidepharm), hexadecyltrimethylammonium bromide (Macklin), 4-dimethylaminopyridine (DMAP, Macklin), N-hydroxysuccinimide (NHS, Macklin), 2′,7′-dichlorofluorescin diacetate (DCFH-DA, Aladdin), DSPE-PEG2000-NH 2 (Yusi), DSPE-PEG2000-FITC (Yusi), cholesterol (Yuanye), trypsin (Macklin), pepsin powder (Bidepharm), bile salts (Macklin), ampicillin (Bidepharm), lysin (Bidepharm), dextran sulfate sodium salt (DSS, MW 40,000, MP Bio), LB nutrient agar (Hopebiol), Cell Counting Kit-8 (CCK-8, Beyotime), mouse IL-6, IFN-γ, IL-1β, and TNF-α uncoated ELISA kits (Thermo Fisher Scientific), and antigen retrieval solution (Servicebio).

Techniques: Drug discovery, Staining, Histopathology, Fluorescence, Incubation, Activity Assay, Enzyme-linked Immunosorbent Assay

Journal: Materials Today Bio

Article Title: Prodrug-integrated multifunctional liposome encapsulation enhances probiotic-based bacteriotherapy for inflammatory bowel disease

doi: 10.1016/j.mtbio.2026.103110

Figure Lengend Snippet: Therapeutic efficacy of DTI@EcN against STm-induced colitis. ( A ) Schematic of the experimental schedule. C57BL/6J mice were pretreated with streptomycin (100 μL, 200 mg/mL) one day prior to oral administration with STm. Afterward, different bacterial formulations were given to mice for 4 days to evaluate their effectiveness against STm-induced colitis. ( B ) Changes in STm counts in feces during the treatment period. ( C ) Quantification of STm per mg of feces on day 4 post-administration of various EcN formulations. ( D ) STm and ( E ) EcN counts in the cecum after different treatments. ( F ) Histological evaluation of colon damage with H&E staining (Scale bar: 100 μm) and ( G ) corresponding histopathology scores, respectively. ( H ) Neutrophil infiltration measured by colonic MPO activity. ( I - L ) Levels of pro-inflammatory cytokines in colon tissues, including IL-6 ( I ), IL-1β ( J ), TNF-α ( K ), and IFN-γ ( L ), as determined by ELISA kits. Data are presented as means ± SEM (n = 5). Statistical analysis was performed using one-way ANOVA. ns: no significance, ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.

Article Snippet: The selected chemicals and biological materials used in this research are as follows: 1-(3-dimethylaminopropyl)-3-ethylcarbodiimide (EDCI, Macklin), 4-bromobutyric acid (Bidepharm), thiourea (Macklin), sodium hydroxide (NaOH, Macklin), hydrochloric acid (HCl, Macklin), trifluoroacetic acid (Bidepharm), idebenone (Bidepharm), hexadecyltrimethylammonium bromide (Macklin), 4-dimethylaminopyridine (DMAP, Macklin), N-hydroxysuccinimide (NHS, Macklin), 2′,7′-dichlorofluorescin diacetate (DCFH-DA, Aladdin), DSPE-PEG2000-NH 2 (Yusi), DSPE-PEG2000-FITC (Yusi), cholesterol (Yuanye), trypsin (Macklin), pepsin powder (Bidepharm), bile salts (Macklin), ampicillin (Bidepharm), lysin (Bidepharm), dextran sulfate sodium salt (DSS, MW 40,000, MP Bio), LB nutrient agar (Hopebiol), Cell Counting Kit-8 (CCK-8, Beyotime), mouse IL-6, IFN-γ, IL-1β, and TNF-α uncoated ELISA kits (Thermo Fisher Scientific), and antigen retrieval solution (Servicebio).

Techniques: Drug discovery, Staining, Histopathology, Activity Assay, Enzyme-linked Immunosorbent Assay

Journal: Genes & Diseases

Article Title: Targeting MDK alleviates bone loss via dual regulation of osteogenic differentiation and inflammatory cytokine expression

doi: 10.1016/j.gendis.2025.101931

Figure Lengend Snippet: iMDK alleviates bone loss via dual regulation of bone formation and inflammatory cytokines. (A) Representative micro-CT images of distal femora (top) with three-dimensional reconstruction of the region of interest (bottom), with the blue indicating higher-density bone and the red indicating lower-density bone. (B – D) Statistical quantification of trabecular bone microstructural parameters (BMD, BV/TV, and Tb.Th). Inter-group comparisons were analyzed by one-way ANOVA. (E) Representative images of trabecular bone area in distal femur sections stained with hematoxylin and eosin. Scale bar, 200 μm or 50 μm. (F) Quantitative analysis of the trabecular bone area of the distal femur stained with hematoxylin and eosin. Inter-group comparisons were analyzed by one-way ANOVA. (G) Immunohistochemical staining of OCN in distal femurs. Scale bar, 200 μm or 50 μm. (H) Quantitative analysis of OCN-positive area. Inter-group comparisons were analyzed by one-way ANOVA. (I) Western blotting analysis of inflammatory cytokine expression (IL-6, TNF-α, and IL-1β) in mouse bone tissues. (J) Inflammatory cytokine expression (IL-6, TNF-α, and IL-1β) in mouse serum was detected by ELISA. Inter-group comparisons were analyzed by one-way ANOVA. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001; “ns” indicates non-significant differences.

Article Snippet: We purchased the Mouse P1NP (Procollagen 1 N-Terminal Propeptide) ELISA Kit (Cat#e-el-m0233), Mouse IL-6 ELISA Kit (Cat#e-el-m0044), Mouse TNF-α ELISA Kit (Cat#e-el-m3063), and Mouse IL-1β ELISA Kit (Cat#e-el-m0037) from Elabscience (Wuhan, China).

Techniques: Micro-CT, Staining, Immunohistochemical staining, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay

Journal: Genes & Diseases

Article Title: Targeting MDK alleviates bone loss via dual regulation of osteogenic differentiation and inflammatory cytokine expression

doi: 10.1016/j.gendis.2025.101931

Figure Lengend Snippet: Recombinant MDK protein triggers the activation of inflammatory cytokines through the NF-κB signaling pathway. (A, B) IL-6, TNFα, and IL-1β expression levels were detected using Western blotting. MC3T3-E1 cells were treated with recombinant MDK protein (600 ng/mL). Osteogenic differentiation was induced for 7 days. Inter-group comparisons were analyzed by a two-tailed unpaired Student's t -test (for normally distributed data with equal variance). (C, D) Western blotting analysis of NF-κB signaling pathway molecules in MC3T3-E1 cells treated with recombinant MDK protein for 7 days during osteoblastic differentiation. Inter-group comparisons were analyzed by two-tailed unpaired Student's t -test (for normally distributed data with equal variance). (E, F) IL-6 and IL-1β expression levels were detected using Western blotting. MC3T3-E1 cells were pretreated with 10 μM BAY 11–7082. Osteogenic differentiation was induced for 7 days. Inter-group comparisons were analyzed by one-way ANOVA. ∗ p < 0.05 and ∗∗ p < 0.01.

Article Snippet: We purchased the Mouse P1NP (Procollagen 1 N-Terminal Propeptide) ELISA Kit (Cat#e-el-m0233), Mouse IL-6 ELISA Kit (Cat#e-el-m0044), Mouse TNF-α ELISA Kit (Cat#e-el-m3063), and Mouse IL-1β ELISA Kit (Cat#e-el-m0037) from Elabscience (Wuhan, China).

Techniques: Recombinant, Activation Assay, Expressing, Western Blot, Two Tailed Test

Journal: Genes & Diseases

Article Title: Targeting MDK alleviates bone loss via dual regulation of osteogenic differentiation and inflammatory cytokine expression

doi: 10.1016/j.gendis.2025.101931

Figure Lengend Snippet: Schematic representation of MDK alleviating bone loss. MDK is significantly elevated in the serum of postmenopausal osteoporotic women and ovariectomized mice. Due to estrogen deficiency, iMDK alleviates bone loss by promoting bone formation and inhibiting inflammatory factors. Recombinant MDK protein inhibits osteogenic differentiation through the PI3K/AKT signaling pathway and up-regulates inflammatory factors IL-6, TNF-α, and IL-1β via the NF-κB signaling pathway.

Article Snippet: We purchased the Mouse P1NP (Procollagen 1 N-Terminal Propeptide) ELISA Kit (Cat#e-el-m0233), Mouse IL-6 ELISA Kit (Cat#e-el-m0044), Mouse TNF-α ELISA Kit (Cat#e-el-m3063), and Mouse IL-1β ELISA Kit (Cat#e-el-m0037) from Elabscience (Wuhan, China).

Techniques: Recombinant

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