Chrysosplenol C
Chrysosplenol C is a type of flavonoid compound. Chrysosplenol C selectively activates cardiac myosin ATPase, with its EC50 being 45 µM. Chrysosplenol C enhances the release of intracellular calcium ions by activating protein kinase C (PKC), thereby increasing the contractility of rat ventricular muscle cells. Chrysosplenol C can be used in the research of heart failure.
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- CAS. Nr.: 23370-16-3
- Formel: C18H16O8
- Molecular Weight:360.31
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
Beschreibung
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| KB | ED50 |
11.2 μg/mL
Compound: chrysosplenol C
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Cytotoxicity against human KB cells after 72 hrs
Cytotoxicity against human KB cells after 72 hrs
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[PMID: 1955888] |
Chemical Information
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CAS. Nr. 23370-16-3
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Molecular Weight 360.31
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Formel C18H16O8
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SMILES
O=C1C(OC)=C(C2=CC(OC)=C(O)C=C2)OC3=CC(OC)=C(C(O)=C13)O
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Structure Classification
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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Calcium Spark Assay
Calcium sparks are localized, transient increases in intracellular calcium concentration ([Ca2+]i) that occur in cardiac myocytes and represent elementary events underlying excitation-contraction coupling. These events are generated by the coordinated opening of clusters of ryanodine receptors (RyRs) on the sarcoplasmic reticulum membrane, leading to a brief release of Ca2+ into the cytosol. The detection and analysis of calcium sparks provide insights into the mechanisms of calcium handling and signaling in cardiac cells. Imaging techniques using fluorescent calcium indicators such as Fluo-3 are employed to visualize these subcellular calcium transients with high spatial and temporal resolution. The protocol is based on established methodologies described in primary literature for both experimental measurement and automated analysis of calcium sparks.
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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
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Ca2+ Staining Technique
Ca2+ staining is an experimental technique that utilizes specific fluorescent probes (such as Fluo-4 AM, Fura-2, etc.) to qualitatively or quantitatively detect dynamic changes in intracellular Ca2+ concentrations; this is achieved by monitoring the changes in fluorescent signals generated when these probes bind to free intracellular calcium ions. The underlying principle relies primarily on the presence of chelating groups within the probe's molecular structure that possess high affinity for calcium ions.
Reinheit & Dokumentation
Verweise
[1]. Venkateswararao E, et al. Exploration of Pharmacophore in Chrysosplenol C as Activator in Ventricular Myocyte Contraction. ACS Med Chem Lett. 2015 May 20;6(7):758-63. [Content Brief]
[2]. Wang J, et al. Chrysosplenol-C Increases Contraction by Augmentation of Sarcoplasmic Reticulum Ca2+ Loading and Release via Protein Kinase C in Rat Ventricular Myocytes. Mol Pharmacol. 2022 Jan;101(1):13-23. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)