Paeonidanin
Paeonidanin is a monoterpenoid glycoside with an IC50 > 100 μM for nitric oxide production inhibition in lipopolysaccharide-activated microglia and macrophages. Paeonidanin suppresses lipopolysaccharide-induced production of nitric oxide, interleukin-6, and tumor necrosis factor alpha in macrophages and microglia.Paeonidanin can be used for the research of inflammation.
For research use only. We do not sell to patients.
- CAS No.: 209969-75-5
- Formula: C24H30O11
- Molecular Weight:494.49
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| N9 | IC50 |
>100 μM
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Inhibition of nitric oxide production in lipopolysaccharide-activated murine N9 microglial cells assessed via Griess reaction after 48 h incubation with Paeonidanin.
Inhibition of nitric oxide production in lipopolysaccharide-activated murine N9 microglial cells assessed via Griess reaction after 48 h incubation with Paeonidanin.
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19691309 |
In Vitro
Paeonidanin (PD) (33 μM; 2 h) potently inhibits LPS-induced NO production in RAW 264.7 cells[1].
Paeonidanin (11-100 μM; 2 h) inhibits LPS-induced TNF-α production in RAW 264.7 cells in a dose-dependent manner, with the strongest effect at 100 μM[1].
Paeonidanin (11-100 μM; 2 h) inhibits LPS-induced IL-6 production in RAW 264.7 cells in a dose-dependent manner, with significant effects at 33 and 100 μM[1].
Paeonidanin (100 μM; 2 h) exhibits no cytotoxicity toward RAW 264.7 cells, with or without LPS stimulation[1].
Paeonidanin (compound 1) (1.0-30.0 μM; 48 h) exhibits weak inhibitory activity on nitric oxide production in LPS-activated N9 microglial cells, with significant inhibition only at 10.0 μM and 30.0 μM, and an IC50 greater than 100 μM[2].
Paeonidanin (compound 11) (> 100 μM) does not inhibit NO production in LPS-induced RAW 264.7 macrophages, with an IC50 > 100 μM[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:RAW 264.7 macrophages
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Concentration:11, 33, 100 μM
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Incubation Time:2 h
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Result:Inhibited LPS-induced TNF-α production in a dose-dependent manner.
Significantly reduced TNF-α production at 33 μM.
Exhibited even stronger inhibition at 100 μM.
Inhibited LPS-induced IL-6 production in a dose-dependent manner.
Significantly reduced IL-6 production at 33 and 100 μM.
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Cell Line:RAW 264.7 macrophages
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Concentration:100 μM
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Incubation Time:2 h
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Result:Showed no obvious cytotoxicity on RAW 264.7 cells at the tested concentration of 100 μM, regardless of LPS stimulation.
Chemical Information
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CAS No. 209969-75-5
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Molecular Weight 494.49
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Formula C24H30O11
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SMILES
O=C(C1=CC=CC=C1)OC[C@@]2([C@@](C(C[C@@]3(O[C@@H]2OC)C)=O)([H])C4)[C@]43O[C@@H]5O[C@@H]([C@H]([C@@H]([C@H]5O)O)O)CO
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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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
Purity & Documentation
References
[1]. Bi X, et al. Anti-Inflammatory Effects, SAR, and Action Mechanism of Monoterpenoids from Radix Paeoniae Alba on LPS-Stimulated RAW 264.7 Cells. Molecules (Basel, Switzerland). 2017 Apr 29;22(5):715. [Content Brief]
[2]. Duan WJ, et al. Monoterpenes from Paeonia albiflora and their inhibitory activity on nitric oxide production by lipopolysaccharide-activated microglia. Journal of natural products. 2009 Sep;72(9):1579-84. [Content Brief]
[3]. Ding L, et al. New monoterpene glycosides from Paeonia suffruticosa Andrews and their inhibition on NO production in LPS-induced RAW 264.7 cells. Bioorganic & medicinal chemistry letters. 2012 Dec 01;22(23):7243-7. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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