Prostaglandin E3
Based on 1 Customer Validation
Prostaglandin E3 is an eicosanoid derived from eicosapentaenoic acid. Prostaglandin E3 inhibits polarization towards M1 but promotes polarization of M2a macrophages. Prostaglandin E3 shows anti-inflammatory and anti-tumor activity.
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- Pureza : 98.4%
- No. CAS: 802-31-3
- Fòrmula: C20H30O5
- Peso molecular:350.45
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Almacenamiento:
Solution, -20°C, 2 years
Actividad biológica
Descripciòn
In Vitro
Prostaglandin E3 (1-10000 nM) suppresses M1 and induces M2a marker expression in polarized macrophages[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
Prostaglandin E3 (1 µmol/L; every 3 days for 4 weeks) shows anti-tumor activity by regulates macrophage polarization[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:5 weeks, Nude mice (BABL/c) (PC3 xenograft model)[1]
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Dosage:1 µmol/L for 50 µL
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Administration:Injected next to the tumour, every 3 days for 4 weeks
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Result:Decreased the weights of transplanted tumours, inhibits the expression of CD68 and CD206.
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Animal Model:6-8-week-old C57BL6/J mice[1]
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Dosage:LPS+ PGE3 (5 mg/kg + 1 µmol/L)
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Administration:I.p.; once
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Result:Significantly reduced MPMs with an M1-like phenotype and increased M2-like MPMs, inhibited inflammatory cytokine secretion in both the serum and MPM cell lysates.
Chemical Information
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No. CAS 802-31-3
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Appearance Liquid
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Peso molecular 350.45
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Fòrmula C20H30O5
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Color Colorless to light yellow
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SMILES
CC/C=C\C[C@H](O)/C=C/[C@@H]1[C@H](C(C[C@H]1O)=O)C/C=C\CCCC(O)=O
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Envío
Room temperature in continental US; may vary elsewhere.
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Almacenamiento
Solution, -20°C, 2 years
Protocolo
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
Pureza y Documentación
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Ficha de datos (275 KB)
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SDS (393 KB)
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Instrucciones de manejo (2659 KB)
Referencias
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)