cxcr2 inhibitor sb225002  (MedChemExpress)

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: AKR1B10 reprograms neutrophils by histone lactylation to foster immune evasion in KRAS G12C mutation colorectal cancer liver metastasis

doi: 10.1186/s13046-026-03653-2

Figure Lengend Snippet: AKR1B10 promotes neutrophil recruitment through the CXCL8/CXCR2 axis. A CT26K cells with AKR1B10 knockdown were analyzed via RNA-seq and KEGG enrichment analysis. B RT-qPCR detected expression of the 6 most pronounced differential genes in the cytokine pathway. C Representative plots and statistical analysis of neutrophil chemotaxis assay. D Schematic diagram of the establish of the CRLM models and the corresponding treatment. E , F Representative fluorescence images (E) and statistical analysis (F) of different CRLM model groups. G Representative gross images and HE images of different CRLM model groups. H , I Liver weight (H) and percentage of liver metastasis foci in the liver (I) of different CRLM model groups. J , K Representative plots and cell proportion of CD8 + T cells (J) and neutrophils (K) of different CRLM model groups. L - N Representative plots and statistical analysis of IFNγ production (L), and surface PD-1 (M), TIM-3 (N) of CD8 + T cells of different CRLM model groups. O Representative plots and statistical analysis of surface PD-L1 of neutrophils of different CRLM model groups

Article Snippet: Treatment of mice included: IgG isotype control), 2 μg intraperitoneal (i.p.) every 2 days; anti-CXCL8 antibodies (Selleck, A2524), 1 mg i.p. every 2 days; CXCR2 inhibitor, SB225002 (Selleck, S7651), 10 mg/kg i.p. every 2 days; anti-Ly6G antibodies (Selleck, A2158), 5 mg/kg i.p. every 2 days; anti-CD8 antibodies (Selleck, A2102), 5 mg/kg i.p. every 2 days; anti-PD-1 antibodies (Selleck, A2122), 10 mg/kg i.p. every 3 days; daily gavage with 0.5% methylcellulose (vehicle group); AKR1B10 inhibitor, Epalrestat (Selleck, S2035) diluted in 0.5% methylcellulose, 50 mg/kg intragastrical (i.g.) every day; and combined therapies: anti-Ly6G antibodies + anti-CD8 antibodies; anti-Ly6G antibodies + anti-PD-1 antibodies and Epalrestat + anti-PD-1 antibodies.

Techniques: Knockdown, RNA Sequencing, Quantitative RT-PCR, Expressing, Chemotaxis Assay, Fluorescence

Journal: Journal of Advanced Research

Article Title: Novel function of macrophage migration inhibitory factor in regulating post-infarct inflammation and the therapeutic significance

doi: 10.1016/j.jare.2025.05.030

Figure Lengend Snippet: Macrophage migration inhibitory factor (MIF) promotes inflammatory cell migration and infiltration through C – C motif chemokine receptor 2 (CCR2) and C-X-C motif chemokine receptor (CXCR) 4 and promotes splenic monocyte mobilization via interaction with angiotensin Ⅱ type 1 receptor (AT-1R) after myocardial infarction (MI). A, peripheral blood mononuclear cells (PBMCs) chemotaxis in response to homogenized sham or infarct heart tissue from wild type (WT) mice at day 3 post-MI, or MI homogenate together with inhibition of C–C motif chemokine receptor 2 (CCR2), C-X-C motif chemokine receptor (CXCR) 2 and CXCR4, respectively. Cells/HPF, cells/high power field. PBMCs harvested from WT mice at 3 days post-MI. CCR2i, CCR2 inhibition. CXCR2i, CXCR2 inhibition. CXCR4i, CXCR4 inhibition. n = 4–8 per group. *** P < 0.001 vs. sham . B, PBMCs chemotaxis in response to recombinant human MIF (rMIF) or rMIF with inhibition of CCR2, CXCR2 and CXCR4, respectively. PBMCs harvested from WT mice at 3 days post-MI. n = 4–8 per group. *** P < 0.001 vs. control . C, Representative immunoblotting images for monocyte chemoattractant protein-1 (MCP-1), CXCR4 and internal reference protein (heat shock protein 60, HSP-60) in hearts from WT and global MIF deficient (MIFKO) mice with sham-operation or 72 h MI. D-E, Quantitative analysis of MCP-1 and CXCR4 expression. n = 6–9 per group. ** P < 0.01 vs. sham in the same genotype. *** P < 0.001 vs. sham in the same genotype. F, Splenic monocyte (from normal WT mice) chemotaxis in response to plasma from normal mice or mice with 1.5 h MI, or MI plasma together with losartan. Lor, losartan, AT-1R inhibitor. n = 6–8 per group. *** P < 0.001 vs. normal. G, Splenic monocytes (from normal WT mice) chemotaxis in response to rMIF and angiotensin II (Ang II), or together with losartan addition, respectively. n = 6–8 per group. ** P < 0.01 vs. Control. *** P < 0.001 vs. Control. H, Representative immunoblotting images for AT-1R and internal reference protein (HSP-60) in spleens from WT and global MIF deficient (MIFKO) mice with sham-operation and 1.5 h MI. I, Quantitative analysis of AT-1R expression. n = 8 per group. *** P < 0.001 vs. sham in the same genotype . J. Co-immunoprecipitation (Co-IP) assay using an anti-AT-1R antibody or IgG demonstrated the interaction between AT-1R and MIF, as well as between AT-1R and CD74 in splenic monocytes and spleen tissue. Input, input sample. IgG, negative control sample. IP, Co-IP sample.

Article Snippet: For both groups 1 and 2, PBMCs were pre-treated for 1 h using DMEM with or without CCR2 inhibitor (CCR2 antagonist 4 hydrochloride, 100 mM), CXCR2 inhibitor (SB225002, 800 nM) or CXCR4 inhibitor (Plerixafor, AMD3100, 10 μM) (all from MedChemExpress, USA).

Techniques: Migration, Chemotaxis Assay, Inhibition, Recombinant, Control, Western Blot, Expressing, Clinical Proteomics, Co-Immunoprecipitation Assay, Negative Control