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MedChemExpress boc 2
Fig. 6 <t>LXA4</t> increased by M2-Exos downregulates CXCR2 and ROS expressions in PMNs. PMNs isolated from healthy volunteers (a and b) or septic patients (d) were activated by septic plasma (SP) and then cocultured with M0/M2-Exos (100 μg/mL) derived from PBMC-differentiated macrophages for 5 h with or <t>without</t> <t>BOC-2</t> (10 µM) incubation. c PMNs from septic patients were directly cocultured with M0/M2-Exos (100 μg/ mL) for 5 h after isolation. CXCR2 (a and c) and ROS (b and d) expressions in cocultured PMNs were detected by flow cytometry. n = 4–5. e and f WT C57BL/6 mice were administered M0/M2-Exos (300 μg/mouse) derived from mouse Raw264.7 macrophages via intraperitoneal injection 1 h after CLP. To block the LXA4 receptor, mice were treated with 50 µg/kg BOC-2 i.p. 30 min before CLP. CXCR2 (e) and ROS (f) expressions in peripheral blood neutrophils were detected by flow cytometry. One-way analysis of variance with Tukey’s multiple comparisons test was used for the analysis. Graphs represent means ± standard deviations, n = 6; *P < 0.05, **P < 0.01 compared within two groups
Boc 2, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Fig. 6 LXA4 increased by M2-Exos downregulates CXCR2 and ROS expressions in PMNs. PMNs isolated from healthy volunteers (a and b) or septic patients (d) were activated by septic plasma (SP) and then cocultured with M0/M2-Exos (100 μg/mL) derived from PBMC-differentiated macrophages for 5 h with or without BOC-2 (10 µM) incubation. c PMNs from septic patients were directly cocultured with M0/M2-Exos (100 μg/ mL) for 5 h after isolation. CXCR2 (a and c) and ROS (b and d) expressions in cocultured PMNs were detected by flow cytometry. n = 4–5. e and f WT C57BL/6 mice were administered M0/M2-Exos (300 μg/mouse) derived from mouse Raw264.7 macrophages via intraperitoneal injection 1 h after CLP. To block the LXA4 receptor, mice were treated with 50 µg/kg BOC-2 i.p. 30 min before CLP. CXCR2 (e) and ROS (f) expressions in peripheral blood neutrophils were detected by flow cytometry. One-way analysis of variance with Tukey’s multiple comparisons test was used for the analysis. Graphs represent means ± standard deviations, n = 6; *P < 0.05, **P < 0.01 compared within two groups

Journal: Journal of biomedical science

Article Title: Exosomal PGE2 from M2 macrophages inhibits neutrophil recruitment and NET formation through lipid mediator class switching in sepsis.

doi: 10.1186/s12929-023-00957-9

Figure Lengend Snippet: Fig. 6 LXA4 increased by M2-Exos downregulates CXCR2 and ROS expressions in PMNs. PMNs isolated from healthy volunteers (a and b) or septic patients (d) were activated by septic plasma (SP) and then cocultured with M0/M2-Exos (100 μg/mL) derived from PBMC-differentiated macrophages for 5 h with or without BOC-2 (10 µM) incubation. c PMNs from septic patients were directly cocultured with M0/M2-Exos (100 μg/ mL) for 5 h after isolation. CXCR2 (a and c) and ROS (b and d) expressions in cocultured PMNs were detected by flow cytometry. n = 4–5. e and f WT C57BL/6 mice were administered M0/M2-Exos (300 μg/mouse) derived from mouse Raw264.7 macrophages via intraperitoneal injection 1 h after CLP. To block the LXA4 receptor, mice were treated with 50 µg/kg BOC-2 i.p. 30 min before CLP. CXCR2 (e) and ROS (f) expressions in peripheral blood neutrophils were detected by flow cytometry. One-way analysis of variance with Tukey’s multiple comparisons test was used for the analysis. Graphs represent means ± standard deviations, n = 6; *P < 0.05, **P < 0.01 compared within two groups

Article Snippet: In addition, some PMNs were cultured with or without 10 μM BOC-2 (LXA4 receptor antagonist; #HY-P1795, MCE corporation, USA), 1 μM PD146176 (15-LO inhibitor; #HY-103157, MCE corporation, USA), 1 μM E7046 (EP4 receptor antagonist; #HY-103088, MCE corporation, USA), 100 nM LXA4 (#90410, Cayman Chemical, Michigan, USA), and 100 nM PGE2 (#HY-101952, MCE corporation, USA).

Techniques: Isolation, Clinical Proteomics, Derivative Assay, Incubation, Flow Cytometry, Injection, Blocking Assay