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    Senegenin
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    CAS No. 2469-34-3 Price $60 / 20mg
    Catalog No.CFN99109Purity>=98%
    Molecular Weight537.14Type of CompoundTriterpenoids
    FormulaC30H45ClO6Physical DescriptionPowder
    Download Manual    COA    MSDS    SDFSimilar structuralComparison (Web)  (SDF)
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    * Packaging according to customer requirements(5mg, 10mg, 20mg and more). We shipped via FedEx, DHL, UPS, EMS and others courier.
    According to end customer requirements, ChemFaces provide solvent format. This solvent format of product intended use: Signaling Inhibitors, Biological activities or Pharmacological activities.
    Size /Price /Stock 10 mM * 1 mL in DMSO / $28.1 / In-stock
    Other Packaging *Packaging according to customer requirements(100uL/well, 200uL/well and more), and Container use Storage Tube With Screw Cap
    Our products had been exported to the following research institutions and universities, And still growing.
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    Senegenin

    Senegenin
    Product Name Senegenin
    CAS No.: 2469-34-3
    Catalog No.: CFN99109
    Molecular Formula: C30H45ClO6
    Molecular Weight: 537.14 g/mol
    Purity: >=98%
    Type of Compound: Triterpenoids
    Physical Desc.: Powder
    Targets: TNF-伪 | IL Receptor | NF-kB | JNK
    Source: The roots of Polygala tenuifolia Willd.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Price: $60 / 20mg
    Inquire / Order: manager@chemfaces.com
    Technical Inquiries: service@chemfaces.com
    Tel: +86-27-84237783
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  • Front Immunol.2020, 11:598556.
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  • Sci Rep. 2018, 462(8)
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  • Srinagarind Medical Journal2019, 34(1)
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  • Int Immunopharmacol.2020, 90:107268.
  • Biomol Ther (Seoul).2019, 10.4062
  • BMC Complement Altern Med.2019, 19(1):339
  • Related Screening Libraries
    Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
    10 mM * 1 mL in DMSO / Inquiry / In-stock
    Related Libraries
  • Neuroprotection Compound Library
  • Anti-sepsis Compound Library
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  • TNF-α Inhibitor Library
  • NF-kB Inhibitor Library
  • JNK Inhibitor Library
  • IL Receptor Inhibitor Library
  • Biological Activity
    Description: Senegenin has anti-apoptotic,anti-oxidative,and neuroprotective activities, it might be a potential agent for prevention and treatment of postoperative cognitive dysfunction (POCD) or other neurodegenerative diseases. It also be a potential therapeutic agent against sepsis. Senegenin decreased the levels of TNF-α ,IL-1β, NF-κB.
    Targets: TNF-α | IL Receptor | NF-kB | JNK
    In vitro:
    Zhong Yao Cai. 2013 Sep;36(9):1477-80.
    Neurotrophic effects of senegenin.[Pubmed: 24620696]
    To study the neurotrophic effects of Senegenin on the expression of MAP2 mRNA and BDNF mRNA in cultured cerebral cortical neurons.
    METHODS AND RESULTS:
    The newborn rat cerebral cortex neurons were cultured in vitro. LDH assay was used to investigate the effect of Senegenin on the neuronal viability and reverse transcription polymerase chain reaction (RT-PCR) was carried out to determine the expression level of MAP2 mRNA and BDNF mRNA. LDH assay showed that Senegenin at the concentration of 0. 5 micromol/L,1 micromol/L and 2 micromol/L could obviously enhance the survival of cells and the survival rates were in dose-dependent manner to some extent. Moreover, the low, medium and high concentrations of Senegenin significantly increased the expression of MAP2 mRNA and BDNF mRNA.
    CONCLUSIONS:
    The study suggests that suitable dose of Senegenin can increase the expression of MAP2 mRNA and BDNF mRNA in cultured cerebral cortical neurons, and its mechanism needs further study.
    In vivo:
    Inflammation. 2016 Apr;39(2):900-6.
    Senegenin Ameliorate Acute Lung Injury Through Reduction of Oxidative Stress and Inhibition of Inflammation in Cecal Ligation and Puncture-Induced Sepsis Rats.[Pubmed: 26945584 ]
    The purpose of this study was to assess the protective effect of Senegenin on acute lung injury (ALI) in rats induced by sepsis.
    METHODS AND RESULTS:
    Rat ALI model was reproduced by cecal ligation and puncture (CLP). All rats were randomly divided into five groups: group 1 (control), group 2 (CLP), group 3 (CLP + Senegenin 15 mg/kg), group 4 (CLP + Senegenin 30 mg/kg), and group 5 (CLP + Senegenin 60 mg/kg). CLP + Senegenin groups received Senegenin by gavage daily for consecutive 5 days, respectively, while the mice in control and CLP groups were given an equivalent volume of saline. We detected the lung wet/dry weight ratios and the histopathology of the lung. The levels of lung tissue myeloperoxidase (MPO), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH) were determined. Meanwhile, the nuclear factor-kappa B (NF-κB) activation, tumor necrosis factor-alpha (TNF-α), and interleukin-1β (IL-1β) levels were studied. The results demonstrated that Senegenin treatment significantly attenuated CLP-induced lung injury, including reduction of lung wet/dry weight ratio, protein leak, infiltration of leukocytes, and MPO activity. In addition, Senegenin markedly decreased MDA content and increased SOD activity and GSH level. Serum levels of TNF-α and IL-1β were also decreased by Senegenin administration. Furthermore, Senegenin administration inhibited the nuclear translocation of NF-κB in the lungs.
    CONCLUSIONS:
    These findings indicate that Senegenin exerts protective effects on CLP-induced septic rats. Senegenin may be a potential therapeutic agent against sepsis.
    Senegenin Description
    Source: The roots of Polygala tenuifolia Willd.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 1.8617 mL 9.3086 mL 18.6171 mL 37.2342 mL 46.5428 mL
    5 mM 0.3723 mL 1.8617 mL 3.7234 mL 7.4468 mL 9.3086 mL
    10 mM 0.1862 mL 0.9309 mL 1.8617 mL 3.7234 mL 4.6543 mL
    50 mM 0.0372 mL 0.1862 mL 0.3723 mL 0.7447 mL 0.9309 mL
    100 mM 0.0186 mL 0.0931 mL 0.1862 mL 0.3723 mL 0.4654 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Protocol
    Cell Research:
    Mol Neurobiol. 2014 Nov 4.
    Senegenin Inhibits Hypoxia/Reoxygenation-Induced Neuronal Apoptosis by Upregulating RhoGDIα[Pubmed: 25367882]
    Neuronal apoptosis is an important event in hypoxia/reoxygenation (H/R)-induced neuronal injury. Senegenin (Sen), the predominant and most active component in Radix Polygalae root extracts, displays anti-apoptotic and anti-oxidative properties. Sen protects against H/R-induced neuronal apoptosis of highly differentiated PC12 cells and primary cortical neurons. Sen has also been investigated as a source of potential therapeutic targets.
    METHODS AND RESULTS:
    In this study, a proteomic approach was used to identify Sen-regulated proteins in PC12 cells. We found that Sen protected against H/R-induced neuronal apoptosis by upregulating RhoGDIα protein expression. The regulatory functions of RhoGDIα were investigated by knocking down RhoGDIα expression in PC12 cells using small interfering RNA (siRNA), followed by quantification of apoptosis and then altering the expression levels of apoptosis-related proteins. Our data show that after silencing RhoGDIα, the neuroprotective effects of Sen on H/R-induced PC12 cell apoptosis were absent. Furthermore, RhoGDIα silencing alleviated the Sen-mediated inhibition of the JNK pathway.
    CONCLUSIONS:
    Therefore, these findings indicated that Sen attenuates H/R-induced neuronal apoptosis by upregulating RhoGDIα expression and inhibiting the JNK pathway. In addition to the mechanism underlying neuroprotective effects of Sen, RhoGDIα was identified as a putative target of Sen based on a primary rat cortical neuron model of H/R-induced injury.
    Animal Research:
    Exp Ther Med. 2014 Apr;7(4):821-826. Epub 2014 Jan 24.
    Protective effect of senegenin on splenectomy-induced postoperative cognitive dysfunction in elderly rats.[Pubmed: 24660030]
    Postoperative cognitive dysfunction (POCD) is common in elderly patients. Senegenin, an active component of extracts from Polygala tenuifolia root, a traditional Chinese medicine, has neuroprotective and neuroregenerative effects. However, the mechanism underlying the effects of Senegenin against postoperative cognitive impairment in elderly individuals has yet to be elucidated.
    METHODS AND RESULTS:
    The aim of this study was to investigate the protective effects of Senegenin on the cognitive functions of elderly rats with splenectomy-induced POCD. Results from a Morris water maze test suggested that splenectomy induced a transient cognitive deficiency in the elderly rats; however, when the rats were treated with Senegenin, the cognitive impairment was notably attenuated. Further experiments showed that Senegenin significantly inhibited the mRNA and protein expression of several key pro-inflammatory cytokines, specifically, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6 and IL-8, in the hippocampal tissues of elderly rats following splenectomy. In order to investigate the molecular mechanism involved, the expression and activity of the Toll-like receptor 4 (TLR4) signaling pathway was assessed. On day 1 postoperatively, it was observed that Senegenin markedly suppressed the mRNA and protein expression of TLR4, myeloid differentiation factor 88 (MyD88) and TIR domain-containing adaptor-inducing interferon-β (TRIF). Furthermore, the phosphorylation levels of nuclear factor-κB (NF-κB) p65 and inhibitor of NF-κB (IκBα) were also decreased following Senegenin treatment on the first day subsequent to surgery. These results suggest that Senegenin suppressed splenectomy-induced transient cognitive impairment in elderly rats, possibly by downregulating two signaling pathways involved in inflammation, TLR4/MyD88/NF-κB and TLR4/TRIF/NF-κB, to further inhibit the expression of key pro-inflammatory cytokines, specifically, TNF-α, IL-1β, IL-6 and IL-8, and ultimately the neuroinflammation in the hippocampal tissues.
    CONCLUSIONS:
    In conclusion, the present study revealed that Senegenin exhibited neuroprotective effects against splenectomy-induced transient cognitive impairment in elderly rats, which indicated that Senegenin may be a promising agent for the treatment of POCD.
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