S-Petasin
S-Petasin is a phosphodiesterase (PDE) inhibitor with IC50 values of 25.5 μM and 17.5 μM for PDE3 and PDE4, respectively. S-Petasin inhibits cholesterol side-chain cleavage enzyme, 11β-hydroxylase, PPAR-γ, and iNOS induction at RNA and protein levels. S-Petasin induces apoptosis, activates caspases, cleaves PARP, modulates mitochondrial membrane permeability, and regulates BCL2/BAX, p53, Bcl-XL, MMP-2, MMP-9, p21, CDK4, and cyclin D1 expression. S-Petasin reduces inflammatory cell accumulation, cytokine and IgE levels, and enhances serum IgG2a levels. S-Petasin relaxes isolated sensitized guinea pig trachealis and exhibits gastrointestinal anti-spasmodic activity. S-Petasin reduces tonsillitis severity and asthmatic attack frequency. S-Petasin can be used for the research of prostate cancer, obesity, melanoma, allergic asthma, asthma, and peritonitis.
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研究用途以外に使用した場合、当社は一切の責任を負いかねます。
- CAS 番号: 70238-51-6
- 分子式: C19H26O3S
- 分子量:334.47
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保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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生物活性
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化学情報
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生物活性
製品説明
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PDE3 25.5 μM (IC50) |
PDE4 17.5 μM (IC50) |
PDE3 25.3 μM (Ki) |
PDE4 18.1 μM (Ki) |
PPARγ |
iNOS |
体外実験
S-Petasin (10 nM-10 μM; 3-4 days) dose-dependently inhibits proliferation of LNCaP, DU145, and PC3 human prostate cancer cells, but not PC3 cells[1].
S-Petasin (0.1-10 μM; 12-18 h) activates caspase cascades and induces PARP cleavage in LNCaP, DU145, and PC3 human prostate cancer cells, consistent with induction of apoptosis[1].
S-Petasin (0.1-10 μM; 8-12 h) induces mitochondrial membrane permeability disruption, cytochrome c release, and modulates expression of BCL2 family proteins and p53 in LNCaP, DU145, and PC3 human prostate cancer cells, triggering mitochondria-mediated apoptosis[1].
S-petasin (0.31-1.55 μM; 8 days) dose-dependently inhibits 3T3-L1 pre-adipocyte differentiation, reducing lipid accumulation to 30.18% at the highest tested concentration[2].
S-petasin (0.31-1.55 μM; 8 days) dose-dependently inhibits triglyceride accumulation in differentiated 3T3-L1 adipocytes, reducing TG content to 61.04% at the highest tested concentration[2].
S-petasin (0.31-1.55 μM) dose-dependently inhibits PPAR-γ expression in 3T3-L1 cells, with greater inhibition observed after 8 days of differentiation treatment than after 24 h[2].
S-petasin (0.31-1.55 μM; 8 days) dose-dependently inhibits the expression of PPAR-γ target genes (HMGCR, FAS, CD36, Glut4, A-FABP, LPL) in differentiated 3T3-L1 adipocytes[2].
S-Petasin (2-160 μM; 24 h) potently inhibits proliferation of B16F10 cells (IC50 = 42.16 μM) and A375 cells (IC50 = 36.90 μM) after 24 h of treatment, as measured by MTT assay[3].
S-Petasin (10-40 μM; 24 h) induces apoptosis of B16F10 cells and A375 cells in a concentration-dependent manner after 24 h of treatment, as measured by Annexin V/PI flow cytometry[3].
S-Petasin (10-40 μM; 24 h) induces apoptosis of B16F10 cells and A375 cells after 24 h of treatment by downregulating pro-apoptotic precursors and upregulating activated cleavage products of caspase 9, caspase 3, and PARP-1[3].
S-Petasin (10-40 μM; 24 h) regulates downstream p53 target genes in B16F10 cells and A375 cells after 24 h of treatment by decreasing nuclear NF-κB, MMP-2, MMP-9, Bcl-2, Bcl-xL, CDK4, and cyclin D1 expression, and increasing Bax and p21 expression, all in a concentration-dependent manner[3].
S-Petasin (4-40 μM; up to 24 h) inhibits migration of B16F10 cells and A375 cells in a concentration-dependent manner over 24 h, as measured by wound healing assay[3].
S-Petasin (4-40 μM; 24 h) inhibits invasion of B16F10 cells and A375 cells through Max Gel ECM in a concentration-dependent manner after 24 h of treatment[3].
S-Petasin (10-40 μM; 24 h) activates p53 expression at mRNA and protein levels in a concentration-dependent manner in B16F10 cells and A375 cells after 24 h of treatment[3].
S-Petasin (1-100 μM; 30 min) competitively inhibits PDE3 and PDE4 from guinea pig lungs and hearts with IC50 values of 25.5 μM and 17.5 μM, respectively, and does not inhibit PDE1, PDE2, or PDE5 at concentrations up to 100 μM[4].
S-Petasin potently inhibits antigen-induced degranulation in RBL-2H3 mast cells with an IC50 of ~1 nM[5].
S-Petasin (1-10 μM; 1 h preincubation, 24 h LPS stimulation) concentration-dependently inhibits LPS-induced iNOS protein and mRNA expression, NO and PGE2 production in mouse peritoneal macrophages, with significant effects at 1, 3, 5, and 10 μM[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:LNCaP, DU145, PC3 (human prostate cancer cell lines)
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Concentration:0.1 μM, 1 μM, 10 μM
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Incubation Time:12, 18 h
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Result:Reduced levels of procaspase 3, 7, 8, and 9 in LNCaP cells after 12 and 18 h.
Reduced levels of procaspase 3, 8, and 9 in DU145 cells after 12 and 18 h (procaspase 7 levels were unchanged).
Reduced levels of procaspase 3, 7, 8, and 9 in PC3 cells after 12 and 18 h.
Induced dose-dependent cleavage of PARP in all three cell lines after 12 and 18 h.
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Cell Line:LNCaP, DU145, PC3 (human prostate cancer cell lines)
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Concentration:0.1 μM, 1 μM, 10 μM
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Incubation Time:8, 12 h
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Result:Increased release of cytochrome c from mitochondria in LNCaP cells after 8 and 12 h.
Increased release of cytochrome c from mitochondria, downregulated BCL2, and downregulated p53 in PC3 cells after 8 and 12 h.
Increased release of cytochrome c from mitochondria, upregulated p53, upregulated BAX, downregulated BCL2, and induced BAX translocation in DU145 cells after 8 and 12 h.
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Cell Line:B16F10 murine melanoma cells, A375 human melanoma cells
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Concentration:10-40 μM
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Incubation Time:24 h
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Result:Increased the proportion of Annexin V and PI positive cells in a concentration-dependent manner in both B16F10 and A375 cells.
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Cell Line:B16F10 murine melanoma cells, A375 human melanoma cells
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Concentration:10 μM, 20 μM, 40 μM
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Incubation Time:24 h
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Result:Decreased expression of pro-caspase 9, pro-caspase 3, and pro-PARP-1, while upregulated expression of cleaved-caspase 9, cleaved-caspase 3, and cleaved-PARP-1 in both B16F10 and A375 cells.\nDecreased nuclear NF-κB expression and suppressed MMP-2 and MMP-9 expression in a dose-dependent manner in both B16F10 and A375 cells.
Downregulated Bcl-2 and Bcl-xL expression, while upregulating Bax expression in a dose-dependent manner in both B16F10 and A375 cells.
Upregulated p21 expression, while suppressing CDK4 and cyclin D1 expression in a dose-dependent manner in both B16F10 and A375 cells.
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Cell Line:B16F10 murine melanoma cells, A375 human melanoma cells
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Concentration:10 μM, 20 μM, 40 μM
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Incubation Time:24 h
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Result:Reduced the number of migrated B16F10 and A375 cells in a dose-dependent manner, with statistically significant inhibition at all tested concentrations.
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Cell Line:B16F10 murine melanoma cells, A375 human melanoma cells
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Concentration:4 μM, 10 μM, 20 μM, 40 μM
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Incubation Time:24 h
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Result:Reduced the number of invaded B16F10 and A375 cells in a dose-dependent manner, with statistically significant inhibition at all tested concentrations.
体内実験
S-Petasin (1 mg/kg; i.p.; 1 h before each ovalbumin nebulization) inhibits ovalbumin-induced accumulation of eosinophils, macrophages, and lymphocytes in BALB/c mouse bronchoalveolar lavage fluid, reducing total cell counts by 80% relative to untreated asthmatic mice[5].
S-Petasin (1 mg/kg; i.p.; single dose 1 h prior to LPS injection) reduces LPS-induced accumulation of total peritoneal cells, polymorphonuclear leukocytes, and mononuclear leukocytes in C57BL/6 mice[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c (female, 8-12 weeks old, allergic asthma model via OVA sensitization and challenge)[4]
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Dosage:10 μmol/kg; 30 μmol/kg
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Administration:s.c.; 2 hours before, 6 and 24 hours after secondary OVA provocation
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Result:Attenuated the enhanced pause (P_enh) value induced by 50 mg/mL methacholine in a dose-dependent and significant manner.
Suppressed increases in total inflammatory cells, neutrophils, and eosinophils in BALF in a significant manner.
Suppressed increases in lymphocytes in BALF at 30 μmol/kg dose, while 10 μmol/kg dose had no effect.
Left macrophage counts in BALF unchanged at both doses.
Suppressed increases in BALF levels of IL-2, IL-5, TNF-α, and IFN-γ in a significant manner at both doses.
Suppressed increases in BALF IL-4 levels at 30 μmol/kg dose, while 10 μmol/kg dose had no effect.
Reversed the reduction in serum total IgG2a levels in a significant manner at 30 μmol/kg dose.
Suppressed increases in serum total IgE, serum OVA-specific IgE, and BALF OVA-specific IgE in a dose-dependent and significant manner at both doses.
Suppressed increases in BALF total IgE levels at 30 μmol/kg dose, while 10 μmol/kg dose had no effect.
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Animal Model:BALB/c (male, 6-week-old, adapted for 1 week prior to experimentation; asthma induced by intraperitoneal ovalbumin + alum on days 1 and 14, nebulized ovalbumin exposure on days 28-30)[5]
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Dosage:1 mg/kg
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Administration:i.p.; 1 h before each ovalbumin nebulization; 3 doses (days 28, 29, 30)
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Result:Blunted ovalbumin-induced increase in total BALF cell number by approximately 80%.
Almost completely inhibited accumulation of macrophages and lymphocytes to PBS-treated basal levels.
Inhibited eosinophil accumulation by approximately 36%.
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Animal Model:C57BL/6 (peritonitis induced by intraperitoneal 1 mg/kg LPS)[5]
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Dosage:1 mg/kg
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Administration:i.p.; single dose 1 h prior to LPS injection
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Result:Reduced total peritoneal cell counts by 36% relative to LPS-induced controls.
Inhibited polymorphonuclear leukocyte accumulation by approximately 37%.
Inhibited mononuclear leukocyte accumulation by approximately 42%.
Did not significantly alter macrophage counts.
- RNA extraction experimental
- Detection of Apoptosis
- TUNEL staining for apoptotic DNA fragmentation
- Mitochondrial membrane-potential fluorescent assay
- Annexin V plus membrane-impermeant dye apoptosis staining
- Ovalbumin-Induced Allergic Airway Inflammation
- Mitochondrial membrane-potential and mitochondrial mass staining
- Zymosan-Induced Peritonitis
- Apoptosis Solutions
- Transepithelial/transendothelial electrical resistance assay
- Research Protocol for Inflammation-related Diseases
- Research Protocol for Metabolic Diseases
化学情報
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CAS 番号 70238-51-6
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分子量 334.47
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分子式 C19H26O3S
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SMILES
C[C@@H]([C@@H](CCC1=CC2=O)OC(/C=C\SC)=O)[C@@]1(C)C[C@H]2C(C)=C
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Structure Classification
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
純度とドキュメンテーション
参考文献
[1]. Wang ZH, et al. Cytotoxic effect of s-petasin and iso-s-petasin on the proliferation of human prostate cancer cells. Anticancer Res. 2015;35(1):191-199. [Content Brief]
[2]. Guo L, et al. S-Petasin isolated from Petasites japonicus exerts anti-adipogenic activity in the 3T3-L1 cell line by inhibiting PPAR-γ pathway signaling. Food Funct. 2019 Jul 17;10(7):4396-4406. [Content Brief]
[3]. Guo L, et al. S-petasin induces apoptosis and inhibits cell migration through activation of p53 pathway signaling in melanoma B16F10 cells and A375 cells. Arch Biochem Biophys. 2020;692:108519. [Content Brief]
[4]. Shih CH, et al. S-Petasin, the Main Sesquiterpene of Petasites formosanus, Inhibits Phosphodiesterase Activity and Suppresses Ovalbumin-Induced Airway Hyperresponsiveness. Evid Based Complement Alternat Med. 2011;2011:132374. [Content Brief]
[5]. Lee KP, et al. Therapeutic effects of s-petasin on disease models of asthma and peritonitis. Biomol Ther (Seoul). 2015;23(1):45-52. [Content Brief]
Calculators
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S-Petasin 関連分類
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