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boc 2  (MedChemExpress)


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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 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hy-p1795/Boc-dPhe-Leu-dPhe-Leu-Phe/pm37533081-78-11-16
    Average 91 stars, based on 2 article reviews
    boc 2 - by Bioz Stars, 2026-10
    91/100 stars

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    1) Product Images from "Exosomal PGE2 from M2 macrophages inhibits neutrophil recruitment and NET formation through lipid mediator class switching in sepsis."

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

    Journal: Journal of biomedical science

    doi: 10.1186/s12929-023-00957-9

    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
    Figure Legend 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

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

    Related Articles

    Cell Culture:

    Article Title: Exosomal PGE2 from M2 macrophage inhibits neutrophil recruitment and NET formation through lipid mediator class switching in sepsis
    Article Snippet: .. In addition, part of PMNs were cultured with or without 10 μM BOC-2 (LXA4 receptor antagonist; #HYP1795, MCE corporation), 1 μM PD146176 (15-LO inhibitor; #HY-103157, MCE corporation), 1 μM E7046 Page 6/29 (EP4 receptor antagonist; #HY-103088, MCE corporation), 100 nM LXA4 (#90410, Cayman Chemical, Michigan, USA), and 100 nM PGE2 (#HY-101952, MCE corporation). .. Transwell assay After treatment with M0/M2-Exo for 5 h, neutrophils (2 × 105) were collected and plated in the upper insert (polycarbonate lter 5 μm) of the transwell kits (#3415, Corning, USA).

    Article Title: Exosomal PGE2 from M2 macrophages inhibits neutrophil recruitment and NET formation through lipid mediator class switching in sepsis.
    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). .. After treatment with M0/M2-Exos for 5 h, neutrophils (2 × 105) were collected and plated in the upper insert (polycarbonate filter 5 μm) of the Transwell kits (#3415, Corning, USA).



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    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
    https://www.bioz.com/product/hy-p1795/Boc-dPhe-Leu-dPhe-Leu-Phe/pm37533081-78-11-16
    Average 91 stars, based on 1 article reviews
    boc 2 - by Bioz Stars, 2026-10
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    n-boc-phe-leu-phe-leu-phe  (MedChemExpress)
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    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
    N Boc Phe Leu Phe Leu Phe, 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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    n-boc-phe-leu-phe-leu-phe - by Bioz Stars, 2026-10
    91/100 stars
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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