Flaccidoside II
Flaccidoside II inhibits proliferation and induces apoptosis in Malignant peripheral nerve sheath tumors (MPNSTs) cell lines. Flaccidoside II ameliorates collagen-induced arthritis in mice. Flaccidoside II is an active triterpenoid saponin constituent from Anemone flaccida rhizome.
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- CAS No.: 140694-19-5
- Formule: C59H96O25
- Masse moléculaire:1205.38
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Chemical Information
- Protocole
- Pureté et documentation
- Références
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Help & FAQs
Activité biologique
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| A-375 | IC50 |
7.3 μM
Compound: 4
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Cytotoxicity against human A375 cells after 72 hrs by sulforhodamine B assay
Cytotoxicity against human A375 cells after 72 hrs by sulforhodamine B assay
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[PMID: 23639650] |
| A549 | IC50 |
10.5 μM
Compound: 4
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Cytotoxicity against human A549 cells after 72 hrs by sulforhodamine B assay
Cytotoxicity against human A549 cells after 72 hrs by sulforhodamine B assay
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[PMID: 23639650] |
| HL-60 | IC50 |
3.2 μM
Compound: 4
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Cytotoxicity against human HL60 cells after 72 hrs by MTT assay
Cytotoxicity against human HL60 cells after 72 hrs by MTT assay
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[PMID: 23639650] |
Chemical Information
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CAS No. 140694-19-5
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Masse moléculaire 1205.38
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Formule C59H96O25
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SMILES
O=C([C@](CC[C@]12C)(CCC3(C)C)[C@](C3)([H])C1=CC[C@@]4([H])[C@]2(CC[C@](C(C)5C)([H])[C@@]4(CC[C@@H]5O[C@H](OC[C@H]6O)[C@@H]([C@H]6O)O[C@H](O[C@H]7C)[C@@H]([C@@H]([C@H]7O)O)O)C)C)O[C@@H]([C@@H]([C@H]8O)O)O[C@@H]([C@H]8O)CO[C@@H]([C@@H]([C@H]9O)O)O[C@@H]([C@H]9O[C@H](O[C@H]%10C)[C@@H]([C@@H]([C@H]%10O)O)O)CO
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Structure Classification
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Initial Source
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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.
Protocole
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Collagen-Induced Arthritis
Collagen-induced arthritis (CIA) is an autoimmune murine model of rheumatoid arthritis in which immunization with type II collagen (CII) emulsified in an adjuvant induces a T cell- and autoantibody-driven inflammatory arthritis characterized by synovial hyperplasia, immune cell infiltration, and joint destruction. The model typically relies on genetically susceptible mouse strains (e. g. , DBA/1) and reproduces key features of human rheumatoid arthritis, including anti-collagen immune responses and progressive joint inflammation. Disease onset generally occurs within ~3-4 weeks after immunization, depending on antigen/adjuvant combinations and protocol variation. The immunopathology is driven by adaptive immune activation against CII, leading to systemic and local joint inflammation mediated by pro-inflammatory cytokines and effector immune cells, making CIA a standard preclinical platform for evaluating immunomodulatory and anti-arthritic interventions.
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Detection of Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
Pureté et documentation
Références
[1]. Zhang GB, et al. Corrigendum to "Flaccidoside II ameliorates collagen-induced arthritis in mice" [Eur. J. Pharmacol. 880 (2020) 173155]. Eur J Pharmacol. 2021 Apr 15;897:173963. [Content Brief]
[2]. Han LT, et al. Triterpenoid saponin flaccidoside II from Anemone flaccida triggers apoptosis of NF1-associated malignant peripheral nerve sheath tumors via the MAPK-HO-1 pathway. Onco Targets Ther. 2016 Apr 5;9:1969-79. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Flaccidoside II Related Classifications
HY-N12141 Related Classifications
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