prostaglandin e2  (Tocris)

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: Frontiers in Pharmacology

Article Title: Crocus sativus L.-derived lauric acid-functionalized gold nanoparticles induce ferroptosis in HeLa cells and reverse M2 macrophage polarization via the PGE2/EP2/cAMP-PKA signaling pathway: a network pharmacology-based study

doi: 10.3389/fphar.2026.1863160

Figure Lengend Snippet: Au@LA reshapes macrophage M1/M2-like polarizationvia the PGE2/EP2/cAMP-PKA signaling axis. (A,B) Flow cytometry analysis of M1 marker iNOS (A) and M2 marker Arg1 (B) expression in CD68 + cells across different treatment groups: PMA, PMA + IL-4, Au@LA alone, Celecoxib (a COX-2 inhibitor, used as a positive control), PGE2 alone, and various combination groups. (C,D) Quantitative analysis of the percentages of iNOS-positive cells (C) and Arg1-positive cells (D) . The results indicate that Au@LA significantly reverses IL-4-induced M2 polarization, while the addition of exogenous PGE2 significantly reverses this protective effect, restoring the M2-like polarization. (E) Western blot analysis of key signaling pathway proteins (PTGER2, p-CREB, CREB, p-PKA, PKA) across the indicated treatment groups. GAPDH was used as the internal loading control. (F–J) Quantitative analysis of relative protein expression levels. Au@LA significantly inhibits the IL-4-induced upregulation of PTGER2 (F) and the phosphorylation of PKA (G) and CREB (H) , whereas exogenous PGE2 reverses these effects. Total levels of PKA (I) and CREB (J) remain unchanged. (K–M) ELISA analysis of PGE2 (K) , IFN-γ (L) , and IL-10 (M) levels in the cell culture supernatant. The results confirm that Au@LA treatment suppresses IL-10 secretion while increasing IFN-γ expression, and this process is regulated by the PGE2 signaling axis, as these effects are rescued by the addition of exogenous PGE2. Data are presented as mean ± SD (n = 3). Statistical significance is indicated by asterisks (*p < 0.05, **p < 0.01, ***p < 0.001).

Article Snippet: When cells were pretreated with Celecoxib (a COX-2 inhibitor, blocking PGE2 synthesis, HY-100579,MedChemExpress, 2 μM) for 1 h, even with the addition of Au@LA, the M2 macrophage proportion remained at a very low 2.8%; conversely, when exogenous PGE2 (HY-101952,MedChemExpress, 10 μM)was supplemented alongside Celecoxib for 48 h, the M2 macrophage proportion significantly rebounded to 7.9%, approaching the model group level.

Techniques: Flow Cytometry, Marker, Expressing, Positive Control, Western Blot, Control, Phospho-proteomics, Enzyme-linked Immunosorbent Assay, Cell Culture