Cinnamic acid sodium
Based on 4 publication(s) in Google Scholar
Cinnamic acid sodium is a orally active naturally occurring aromatic fatty acid of low toxicity. Cinnamic acid sodium shows neuroprotective and anti-inflammatory effects.
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- CAS No.: 538-42-1
- Formule: C9H7NaO2
- Masse moléculaire:170.14
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications Citing Use of MedChemExpress (MCE) Cinnamic acid sodium
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Activité biologique
Description
In Vitro
Cinnamic acid sodium (0.05, 0.4, 3.2 mM; 6, 12, 24 h) induces apoptosis in HT-144 cells in 3.2 mM at 24 h[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:NGM, HT-144 cells
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Concentration:0.05, 0.4, 3.2 mM
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Incubation Time:6, 12, 24 h
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Result:Induced apoptosis in HT-144 cells in 3.2 mM at 24 h, no effect apoptosis in NGM cells.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:6-8 weeks, C57BL/6 mice (18 mg/kg MPTP-HCl, i.p.; at 2-h intervals for 4 times)[1]
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Dosage:100 mg/kg
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Administration:Gavage; starting from 3 h after the last injection of MPTP
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Result:Protected nigral TH levels, protected striatal innervation and neurotransmitters, restored locomotor deficit, increased the activation of Peroxisome Proliferator-Activated Receptor alpha (PPARα) in primary mouse astrocytes, protected striatal TH via PPARα.
Chemical Information
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CAS No. 538-42-1
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Masse moléculaire 170.14
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Formule C9H7NaO2
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SMILES
O=C(O[Na])/C=C/C1=CC=CC=C1
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (4)
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Journal Impact Factor
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Most Recent
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J Neurosci
2025 Aug 27;45(35):e0523252025. PMID: 40769725 -
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Protocole
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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
Pureté et documentation
Références
[1]. Prorok T, et al. Cinnamic Acid Protects the Nigrostriatum in a Mouse Model of Parkinson's Disease via Peroxisome Proliferator-Activated Receptorα. Neurochem Res. 2019 Apr;44(4):751-762. [Content Brief]
[3]. Niero EL, et al. Cinnamic acid induces apoptotic cell death and cytoskeleton disruption in human melanoma cells. J Exp Clin Cancer Res. 2013 May 23;32(1):31. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)