ifn γ  (MedChemExpress)

Journal: Cell Reports Medicine

Article Title: A biomimetic hybrid membrane vesicle nanoplatform attenuates tendinopathy through neuroinflammation modulation and tendon regeneration

doi: 10.1016/j.xcrm.2026.102937

Figure Lengend Snippet: MSM-DTM adsorbs inflammatory cytokines, suppresses TSPCs inflammation and senescence, and promotes tenogenic differentiation and migration (A) The remaining concentrations of TNF-α, IL-1β, IL-6, IFN-γ, LPS, and NGF were detected by ELISA after co-culture with different concentrations of MSM. (B and C) RT-qPCR of IL-6 and CCL-2 in TSPCs under different treatments. (D) Western blot of COL1A2, MMP3, and TNMD. (E) ELISA of TNF-α, IL-6, and IFN-γ in supernatants. (F)Western blot of p16 and p21 after 7 days of treatment. (G) β-Galactosidase staining analysis after 7 days of treatment. Scale bars, 100 μm. (H and I) Immunofluorescence and quantification of TNMD and TNC after 14-day treatment. Scale bars, 50 μm. (J) Relative mRNA expression of tenogenic differentiation markers SCX and TNC. (K and L) Representative images and quantification of Transwell assay. Scale bars, 100 μm. (M and N) Representative images and quantification of wound healing assay. Scale bars, 100 μm. Statistical comparisons were performed with one-way ANOVA with Tukey’s multiple comparisons test. Data are presented as the mean ± SD, n = 3. Ns, no significance, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 between groups.

Article Snippet: IFN-γ ELISA kit , ABclonal , RK00015.

Techniques: Migration, Enzyme-linked Immunosorbent Assay, Co-Culture Assay, Quantitative RT-PCR, Western Blot, Staining, Immunofluorescence, Expressing, Transwell Assay, Wound Healing Assay

Journal: Cell Reports Medicine

Article Title: A biomimetic hybrid membrane vesicle nanoplatform attenuates tendinopathy through neuroinflammation modulation and tendon regeneration

doi: 10.1016/j.xcrm.2026.102937

Figure Lengend Snippet:

Article Snippet: IFN-γ ELISA kit , ABclonal , RK00015.

Techniques: Recombinant, Lysis, Hydroxyproline Assay, Enzyme-linked Immunosorbent Assay, Isolation, SYBR Green Assay, Bicinchoninic Acid Protein Assay, Staining, Software

Journal: Advanced Science

Article Title: Senkyunolide I Inhibits mtDNA‐cGAS‐STING Signaling in Macrophages via Targeting VDAC1 Oligomerization to Attenuate Ulcerative Colitis

doi: 10.1002/advs.77045

Figure Lengend Snippet: ABPP proteomic analysis confirms VDAC1 as target protein of SEI. (A) Chemical structures of SEI and SEI probe (SEI‐P). (B) Cell viability of iBMDM cells treated with SEI or SEI‐P. (C) Release of inflammatory cytokine IL‐1β and (D) cell viability in TNF‐α plus IFN‐γ‐induced iBMDM cells. (E) Cellular imaging of SEI‐P with different exposure times in iBMDM cells. (F) Dose‐dependent labeling of proteins by SEI‐P in iBMDM cells. (G) Competition between SEI and SEI‐P for protein binding in situ (red star: 35 kD). (H) Chemical proteomics analysis workflow for identifying potential targets of SEI, created using Figdraw. (I) Volcano plot of proteins identified in the ABPP method. The graph displayed the log 2 FC of the competition group (100 µ m SEI + 50 µ m SEI‐P) versus SEI‐P (50 µ m ) ( x ‐axis) against the −log 10 ( p‐ value) ( y ‐axis). Among these, points with p < 0.05 and log 2 FC < −1 (blue) were selected as target protein candidates. Values were expressed as mean ± SD ( n = 3).

Article Snippet: Senkyunolide I (HY‐N0745), Erastin (HY‐15763), H‐151 (HY‐112693), TNF‐α (HY‐P7058 or HY‐P7090), IFN‐γ (HY‐P7025 or HY‐P7071), Lipopolysaccharides (LPS, HY‐D1056), Adenosine 5'‐triphosphate (ATP, HY‐B2176) were purchased from MedChem Express.

Techniques: Imaging, Labeling, Protein Binding, In Situ

Journal: Advanced Science

Article Title: Senkyunolide I Inhibits mtDNA‐cGAS‐STING Signaling in Macrophages via Targeting VDAC1 Oligomerization to Attenuate Ulcerative Colitis

doi: 10.1002/advs.77045

Figure Lengend Snippet: SEI directly interacts with VDAC1 to inhibit its oligomerization. (A) The interaction between SEI and VDAC1 was detected using molecular docking. (B) Lysates from iBMDM cells were incubated with or without SEI (100 µ m ) for 24 h. Different concentrations of pronase E were added for 20 min, and VDAC1 content was analyzed using WB analysis. (C) Lysates from iBMDM cells were incubated with SEI at the indicated concentrations for 24 h, with a final concentration of 0.01% pronase E added for 20 min. The level of VDAC1 was assessed through WB analysis. (D) iBMDM cells were incubated with SEI (100 µ m ) for 24 h. These samples were then analyzed using CETSA. Values were expressed as mean ± SD ( n = 3). * p < 0.05, ** p < 0.01 versus SEI group. (E) MST demonstrating a direct interaction between SEI and EGFP‐tagged VDAC1 in lysates from EGFP‐VDAC1 expressing HEK293T cells. (F) Immunoblotting analysis of VDAC1 cross‐linking in iBMDM cells, untreated or stimulated with TNF‐α plus IFN‐γ, with or without addition of SEI (100 µ m ). (G) The VDAC1‐OE plasmid was transfected into iBMDM cells, and cGAMP production was subsequently measured by ELISA. (H) iBMDM cells were transfected with VDAC1‐OE, and then the phosphorylation levels of STING and IRF3 were measured by WB. (I) The mRNA expression levels of CCL5 , CXCL10 , and ISG15 in iBMDM cells transfected with VDAC1‐OE were measured by qRT‐PCR. (J) qRT‐PCR analysis of cytoplasmic mtDNA ( mt‐Nd1 , D‐loop and mt‐Cytb ). Values were expressed as mean ± SD ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Senkyunolide I (HY‐N0745), Erastin (HY‐15763), H‐151 (HY‐112693), TNF‐α (HY‐P7058 or HY‐P7090), IFN‐γ (HY‐P7025 or HY‐P7071), Lipopolysaccharides (LPS, HY‐D1056), Adenosine 5'‐triphosphate (ATP, HY‐B2176) were purchased from MedChem Express.

Techniques: Incubation, Concentration Assay, Expressing, Western Blot, Plasmid Preparation, Transfection, Enzyme-linked Immunosorbent Assay, Phospho-proteomics, Quantitative RT-PCR

Journal: Advanced Science

Article Title: Senkyunolide I Inhibits mtDNA‐cGAS‐STING Signaling in Macrophages via Targeting VDAC1 Oligomerization to Attenuate Ulcerative Colitis

doi: 10.1002/advs.77045

Figure Lengend Snippet: SEI directly binds to K12 on VDAC1. (A) The RMSD of the VDAC1 backbone was simulated for a range of 100 ns. (B) The RMSF values of all amino acid residues were simulated. (C) Radius of gyration of the apo (blue) and protein when bound to the ligand (red) for the 100 ns simulation. (D) DCCM analysis matrix of VDAC1 protein; the region in red indicates residue pairs in horizontal and vertical coordinates have positive correlation in movement patterns, while the region in blue indicates negative correlation. (E) DCCM analysis matrix of SEI‐VDAC1 complex. (F–H) Movement correlation of each residue with a negative correlation coefficient ranged from −0.6 to −0.8 of VDAC1 protein (F), ranged from −0.4 to −0.6 of VDAC1 protein (G), and ranged from −0.4 to −0.6 of SEI‐VDAC1 complex (H). (I) The total binding free energy was calculated, and a series of contribution components were analyzed. Data are presented as energy changes in units of kJ/mol. (J) Ten residues of the VDAC1‐SEI complex were selected and analyzed. Data were presented as energy changes in a unit of kJ/mol with different contributors indicated by colors. (K) Free energy landscape. (L) Sequence conservation analysis of VDAC1 protein using ESPript 3.0. (M) The iBMDM cells were transfected with K174, K12, and G172 mutation plasmids and then treated with DMSO or SEI (100 µ m ) for 1 h. The interaction between SEI and VDAC1 was detected using the CETSA assay. Values were expressed as mean ± SD ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001 versus Ctrl group. (N) VDAC1 −/− iBMDM cells were transfected with Flag‐VDAC1(WT), Flag‐VDAC1(K174A), Flag‐VDAC1(K12A), or Flag‐VDAC1(G172A). Immunoblotting analysis of VDAC1 cross‐linking in iBMDM cells stimulated with TNF‐α plus IFN‐γ, with or without addition of SEI (100 µ m ). (O) VDAC1 −/− iBMDM cells were transfected with an empty vector, Flag‐VDAC1‐WT, Flag‐VDAC1(K174A), Flag‐VDAC1(K12A), or Flag‐VDAC1(G172A). WB analyses of the quantity of p‐TBK1 and p‐IRF3 after stimulation with TNF‐α plus IFN‐γ and treatment with SEI (100 µ m ) or left untreated (control) for 24 h. Values were expressed as mean ± SD ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Senkyunolide I (HY‐N0745), Erastin (HY‐15763), H‐151 (HY‐112693), TNF‐α (HY‐P7058 or HY‐P7090), IFN‐γ (HY‐P7025 or HY‐P7071), Lipopolysaccharides (LPS, HY‐D1056), Adenosine 5'‐triphosphate (ATP, HY‐B2176) were purchased from MedChem Express.

Techniques: Residue, Binding Assay, Sequencing, Transfection, Mutagenesis, Western Blot, Plasmid Preparation, Control

Journal: Oncology Letters

Article Title: CD47 monoclonal antibody enhances the inhibitory effect of anti-HER2 chimeric antigen receptor macrophages on ovarian cancer

doi: 10.3892/ol.2026.15711

Figure Lengend Snippet: CD47 mAb enhances the pro-inflammatory polarization of anti-HER2 CAR-Ms. (A) Flow cytometry analysis and (B) quantification of the effect of CD47 mAb on CD86 expression on the surface of anti-HER2 CAR-Ms (n=3). PE-CD86 indicates that a PE-channel flow cytometry antibody was used to detect the CD86-positive cell population. (C) Flow cytometry analysis and (D) quantification of the effect of CD47 mAb on CD206 expression of anti-HER2 CAR-Ms (n=3). APC-CD206, indicates that an APC-channel flow cytometry antibody was used to detect the CD206-positive cell population. ELISA results showing the effect of CD47 antibody on the secretion of inflammatory cytokines (E) IFN-γ, (F) TNF-α, (G) IL-6 and (H) IL-1β by CAR-Ms (n=3). CAR-M, chimeric antigen receptor macrophage; mAb, monoclonal antibody.

Article Snippet: The concentrations of IFN-γ (cat. no. ELH-IFNg; RayBio, Inc.), TNF-α (cat. no. ELH-TNFα; RayBio, Inc.), IL-6 (cat. no. KIT10395A; Sino Biological, Inc.) and IL-1β (cat. no. EL-H0149; Wuhan Elabscience Biotechnology Co., Ltd.) in the supernatant of the co-culture system were detected by ELISA kits, according to the manufacturer's instructions.

Techniques: Flow Cytometry, Expressing, Enzyme-linked Immunosorbent Assay

Journal: EMBO Reports

Article Title: Human ZBP1 is a potent inducer of cell death through mechanisms divergent from mouse ZBP1

doi: 10.1038/s44319-026-00866-6

Figure Lengend Snippet: Reagents and tools table

Article Snippet: Recombinant Human IFN-γ , ABclonal , Cat#RP01038.

Techniques: Recombinant, Sequencing, Magnetic Beads, Protease Inhibitor, Software, Microscopy, Bicinchoninic Acid Protein Assay