pge2  (Cayman Chemical)

Journal: Bioactive Materials

Article Title: Mesenchymal stromal cells-loaded 3D radially aligned composite scaffold with potentiated paracrine signaling for sequential bone regeneration

doi: 10.1016/j.bioactmat.2026.02.059

Figure Lengend Snippet: Temporal analysis of the BMSC paracrine profile on different scaffolds. (A) Confocal microscopy images from Live/Dead fluorescence staining of BMSCs encapsulated within the PCL/HAp-GelMA/BMSCs scaffold after 1, 3, 5, and 14 d of 3D culture (live cells, green; dead cells, red). (B) The concentrations of key paracrine factors (TGF-β, PGE2, VEGF, HGF, and BMP-2) from BMSCs cultured in different scaffolds, quantified from culture supernatants at day 3 and day 7. (C) Corresponding relative mRNA expression levels of TGFB1, PTGS2, VEGFA, HGF, and BMP-2 in BMSCs at day 3 and day 7, as determined by qPCR analysis. Data are presented as mean ± SD (n = 3) *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001; ns: not significant.

Article Snippet: ELISA kits for PGE2 (Cat. No. E-EL-0034), TGF-β (Cat. No. E-EL-0162), VEGF (Cat. No. E-EL-R2603), and HGF (Cat. No. E-EL-R0496) were purchased from Elabscience (Wuhan, China).

Techniques: Confocal Microscopy, Fluorescence, Staining, Cell Culture, Expressing

Journal: Bioactive Materials

Article Title: Chronic inflammation-responsive hydrogel restores myeloid-T cell crosstalk to reinvigorate antitumor immunity against metastatic colorectal cancer

doi: 10.1016/j.bioactmat.2026.03.012

Figure Lengend Snippet: PGE2 blockade modulates immune cell phenotypes in antitumor resp onses. (A) Inflammatory gene expression across cancer types (GEPIA2 database). (B) Gene expression of Il1b , Cxcl8 , and Lif in colon adenocarcinoma (COAD) tumor tissue and normal tissue (GEPIA2 database). (C and D) Correlation between Ptgs2 and inflammatory genes in various cancers (C) and COAD (D) (TIMER 2.0). (E) Schematic of immune cells co-incubated with CXB treated tumor conditional medium (TCM) (Source material from BioRender). (F and G) Cell viability (F) and Cell cycle arrest (G) detection of CT26 tumor cells treated with gradient concentrations of CXB; n = 3. (H) PGE2 concentration in CT26 cell supernatants; n = 3. (I) The proportion of CD103 + DC within BMDCs after CXB treatments in vitro ; n = 3. (J and K) Maturation (J) and Antigen processing capability (K) on BMDCs; n = 3. (L – N) Flow charts of CD86 or CD206 expression on Raw 264.7 cells (L). Quantification of CD86 (M) and CD206 (N) expression on Raw 264.7 cells; n = 3. (O and P) Flow charts (O) and Quantification (P) of CD69 and CD137 expression on splenic T cells exposed to CXB-pretreated TCM; n = 3. (Q) IFN-γ secretion by T cells co-cultured with CXB-pretreated TCM; n = 3. Data are presented as mean ± SD, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Significance was calculated using One-way ANOVA.

Article Snippet: ELISA kits for mouse IL-1β, IL-6, IL-12p70, TNFα (BioLegend, USA), PGE2 (Cayman Chemical Company, USA), IL-2 (Dakewe Biotech, Shenzhen, China), IFN-γ, and TGF-β (Invitrogen, Thermo Fisher Scientific, USA) were used for cytokine quantification.

Techniques: Gene Expression, Incubation, Concentration Assay, In Vitro, Expressing, Cell Culture

Journal: Bioactive Materials

Article Title: Chronic inflammation-responsive hydrogel restores myeloid-T cell crosstalk to reinvigorate antitumor immunity against metastatic colorectal cancer

doi: 10.1016/j.bioactmat.2026.03.012

Figure Lengend Snippet: Sustained PGE2 blockade prompts immune activ ation. (A) Structure of hydrogel matrix and scheme of Gel-CXB preparation (Source material from BioRender). (B) Microstructure of the hydrogel. (C) Rheological evaluation of Gel-CXB. (D) CXB release from Gel-CXB in PBS or PBS containing 0.5 mM H 2 O 2 ; n = 3. (E and F) Flow chart (E) and Quantification (F) of CD103 + DC within BMDCs; n = 3. (G and H) Flow chart (G) and Heatmap (H) of costimulatory molecular expression on CD103 - DC, CD103 + DC, or total DC with different treatments; n = 3. (I and J) CXCL9 (I) and Costimulatory molecular expression (J) on cDC1; n = 3. (K – M) CD86 and CD206 expression (K), MHC-II expression (L), and Antigen processing capability (M) of BMDMs incubated with different TCM; n = 3. (N and O) CD69 (N) and CD137 (O) expression on CD8 + T cells co-incubated with different TCM; n = 3. (P) Scheme of Gel-CXB-regulated CT26 TME at different time points in vivo . (Q) Changes of several immune cells within TME at Day 1, 5, and 9; n = 3. (R) Tumor volume of mice treated with CXB alone or Gel-CXB in vivo ; n = 5. (S) CD137 expression on CD8 + T cells in vivo ; n = 3. Data are presented as mean ± SD, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Significance was calculated using One-way ANOVA.

Article Snippet: ELISA kits for mouse IL-1β, IL-6, IL-12p70, TNFα (BioLegend, USA), PGE2 (Cayman Chemical Company, USA), IL-2 (Dakewe Biotech, Shenzhen, China), IFN-γ, and TGF-β (Invitrogen, Thermo Fisher Scientific, USA) were used for cytokine quantification.

Techniques: Expressing, Incubation, In Vivo

Journal: Bioactive Materials

Article Title: Sulfated polysaccharide prevents senescent adipocyte-driven osteonecrosis by stem cell fate reprogramming

doi: 10.1016/j.bioactmat.2025.11.039

Figure Lengend Snippet: SCS reprograms the lineage commitment of MSCs after GC treatment and inhibits the generation of primary senescent adipocytes. ( A ) Schematic illustration of the in vitro investigation of SCS targeting the prostaglandin/PPARγ/INK positive feedback loop in MPS-induced primary senescent adipocytes. ( B ) Representative flow cytometry plot showing p16 + senescent cells in adipocytes derived from bone marrow after 14 days of in vivo MPS induction and subsequently treated with SCS in vitro . ( C ) qPCR analysis of 12 senescence-associated markers in primary senescent adipocytes after in vitro SCS treatment. n = 3 biological replicates. ( D ) ELISA analysis of IL-1β levels in adipocyte supernatant following in vitro SCS treatment. n = 6 biological replicates. ( E ) ELISA analysis of secreted prostaglandins PGD2 and PGE2 in adipocytes under different treatment conditions. D-PBS: bone marrow adipocytes isolated from mice treated in vivo with the solvent control DMSO, followed by in vitro treatment with PBS; M-PBS: bone marrow adipocytes isolated from mice treated in vivo with MPS, followed by in vitro treatment with PBS. M-SCS: bone marrow adipocytes isolated from mice treated in vivo with MPS, followed by in vitro treatment with SCS. ( F ) Western blot analysis of intracellular COX-2 protein levels in adipocytes across the three treatment conditions. ( G ) Schematic illustration of competitive osteogenic–adipogenic differentiation of CD45 − Ter119 − CD31 − LepR + MSCs after 7 days of in vivo SCS and MPS co-treatment. ( H ) qPCR analysis of pan-adipocyte markers ( Fabp4 , Adipoq , Plin1 , Cd36 , and Lep ) in CD45 − Ter119 − CD31 − LepR + MSCs after 14 days of in vitro competitive lineage differentiation. n = 3 biological replicates. ( I and J ) Representative immunofluorescence images (I) and quantification (J) of perilipin + adipocytes and osteopontin + mature osteoblasts derived from lineage-committed MSCs. n = 6 biological replicates. (Scale bars, 30 μm, 15 μm and 15 μm). ( K ) Western blot analysis of adipogenesis-related markers C/EBPα, PPARγ, and C/EBPβ in the lineage-mixed cells after in vitro competitive differentiation of CD45 − Ter119 − CD31 − LepR + MSCs. ( L ) qPCR analysis of lipogenesis-related markers Fasn , Scd1 , Srebf1 , Acaca , and Acacb . n = 3 biological replicates. ( M and N ) Representative H&E staining images (M) of the femurs at day 14 following SCS and MPS co-treatment. Yellow arrows indicate bone marrow adipocytes. Magnified images show hypertrophic adipocyte morphology, with quantification of adipocyte diameter (N). n = 19 biological replicates. (Scale bars, 200 μm, 50 μm and 20 μm). Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; ns, not significant. Statistical significance was determined using an unpaired two-tailed Student's t -test ( C, D, H, J, L and N ), or one-way ANOVA with Tukey's post hoc test ( E ).

Article Snippet: To further investigate the anti-senescent effects of SCS on primary senescent adipocytes, ELISA was performed on adipocyte supernatant to quantify senescence-associated factors including IL-1β (Neobioscience, EMC001b.96), IL-18 (Neobioscience, EMC011.96), TNF-α (Neobioscience, EMC102a.96), and prostaglandins PGJ2 (NOVUS, NBP2-61285), PGD2 (Cayman Chemical, 500151), and PGE2 (R&D Systems, KGE004B).

Techniques: In Vitro, Flow Cytometry, Derivative Assay, In Vivo, Enzyme-linked Immunosorbent Assay, Isolation, Solvent, Control, Western Blot, Immunofluorescence, Staining, Two Tailed Test

Journal: bioRxiv

Article Title: OmpA controls intracellular survival of Acinetobacter baumannii through TFEB activation and lysosomal remodeling

doi: 10.64898/2026.04.18.719357

Figure Lengend Snippet: (A) Immunostaining of iPLA 2 in HeLa cells infected with the ATCC 17978 strain for 24 h. (B) Immunoblot analysis of inactive and active forms of iPLA 2 in HeLa cells infected with the ATCC 17978 strain for 24 h. (C) Enzymatic activity of iPLA 2 in HeLa cells infected with the ATCC 17978 strain for 24 h, in the presence or absence of BEL. * P =0.025 for ATCC 17978 vs. CTL, ** P =0.05 for ATCC 17978 vs. ATCC 1797 8 + BEL (5 µM), *** P =0.042 for ATCC 17978 vs. ATCC 17978 + BEL (10 µM). (D) Cox-2 enzymatic activity in HeLa cells infected with the ATCC 17978 strain for 24 h, in the presence or absence of BEL and NS. (* P =0.0011 for ATCC 17978 vs. CTL, * P =0.049 for CTL vs. ATCC 17978 + BEL (5 µM), * P =0.0096 for CTL vs. ATCC 17978 + NS, ** P =0.0005 for ATCC 17978 vs. ATCC 17978 + BEL (5 µM), *** P =0.001 for ATCC 17978 vs. ATCC 17978 + NS. ( E ) PGE2 production in HeLa cells infected with the ATCC 17978 strain for 24 h, in the presence or absence of BEL and NS. * P =0.004 for ATCC 17978 vs. CTL, ** P =0.0417 for ATCC 17978 vs. ATCC 17978 + BEL (5 µM), *** P =0.0015 for ATCC 17978 vs. ATCC 17978 + NS. CTL: control; Str: staurosporine; BEL: bromoelone lactone; NS: cyclooxygenase inhibitor; Cox-2: cyclooxygenase-2; PGE2: prostaglandin 2.

Article Snippet: Prostaglandin E2 (PGE2) levels were quantified in three independent experiments using the PGE2-EIA monoclonal kit (Cayman Chemical, USA) from culture supernatants collected after the same treatments.

Techniques: Immunostaining, Infection, Western Blot, Activity Assay, Control