Sargachromanol E
Sargachromanol E is an apoptosis inducer, anti-inflammatory agent, and anti-aging agent. Sargachromanol E activates caspase-3, mediates PARP cleavage, downregulates Bcl-xL and upregulates Bax levels, and drives sub-G1 phase cell cycle arrest, inhibits LPS-induced COX-2 and iNOS transcription and expression (NO: IC50 = 6.99 μg/mL), reduces p38 MAPK and ERK1/2 phosphorylation levels, and suppresses the release of pro-inflammatory mediators such as TNF-α, IL-1β, and prostaglandin E2 (PGE2). Sargachromanol E can be used for research on skin aging, leukemia, oral squamous cell carcinoma, and inflammation-related studies.
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- CAS No.: 856414-54-5
- 화학식: C27H40O4
- 분자량:428.60
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보관:
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
- 순도&문서
- References
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Help & FAQs
All Caspase Isoforms
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Biological Activity
제품 설명
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iNOS 6.99 μg/mL (IC50) |
Caspase-3 |
Bcl-xL |
Bax |
COX-2 |
p38 MAPK |
ERK1 |
ERK2 |
IL-1β |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| RAW264.7 | IC50 |
6.99 μg/mL
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Inhibition of nitric oxide (NO) production in LPS-stimulated murine RAW 264.7 macrophages, assessed via Griess reaction after 2 h pretreatment with sargachromanol E followed by 24 h LPS incubation.
Inhibition of nitric oxide (NO) production in LPS-stimulated murine RAW 264.7 macrophages, assessed via Griess reaction after 2 h pretreatment with sargachromanol E followed by 24 h LPS incubation.
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23973192 |
| RAW264.7 | IC50 |
16.3 μM
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Inhibition of lipopolysaccharide-induced nitric oxide production in murine RAW 264.7 macrophages.
Inhibition of lipopolysaccharide-induced nitric oxide production in murine RAW 264.7 macrophages.
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35539527 |
In Vitro
Sargachromanol E (SE) (12.5-50 μM; 24 h) potently inhibits the proliferation of human promyelocytic leukemia HL-60 cells in vitro in a dose-dependent manner, with inhibition rates of 10.7%, 68.9% and 90.1% at concentrations of 12.5, 25 and 50 μM, respectively, and exhibits no cytotoxicity against normal cell lines at these concentrations[1].
Sargachromanol E (12.5-50 μM; 24 h) induces nuclear pyknosis and fragmentation in human promyelocytic leukemia HL-60 cells[1].
Sargachromanol E (12.5-50 μM; 24 h) induces apoptotic DNA fragmentation in human promyelocytic leukemia HL-60 cells[1].
Sargachromanol E (12.5-25 μM; 24 h) regulates the expression of apoptosis-related proteins in human promyelocytic leukemia HL-60 cells; at concentrations of 12.5 μM and 25 μM, slight upregulation of Bax, significant downregulation of Bcl-xL, activation of caspase-3 and caspase-9, and cleavage of PARP are observed[1].
Apoptosis induced by Sargachromanol E (25 μM; 24 h) in human promyelocytic leukemia HL-60 cells is attenuated by the caspase-3 inhibitor Z-DEVD-fmk (HY-12466)[1].
Sargachromanol E (12.5-50 μM; 24 h) induces a concentration-dependent increase in apoptotic sub-G1 hypodiploid cells without affecting the progression of the G2/M phase in human promyelocytic leukemia HL-60 cells[1].
Sargachromanol E (5-25 μg/mL; pre-treatment for 2 h) potently inhibits NO production in LPS-stimulated RAW 264.7 macrophages, with an IC50 of 6.99 μg/mL, and shows no cytotoxicity even at concentrations as high as 25 μg/mL[2].
Sargachromanol E (16.3 μM) inhibits NO production in LPS-stimulated mouse RAW 264.7 macrophages, with an IC50 value of 16.3 μM[4].
Sargachromanol E (5-25 μg/mL; pre-treatment for 2 h) dose-dependently inhibits the production of PGE2, TNF-α, and IL-1β, reduces the protein expression of COX-2 and iNOS, suppresses the phosphorylation of ERK1/2 and JNK, and mildly decreases the phosphorylation of p38 in LPS-stimulated RAW 264.7 macrophages[2].
Sargachromanol E induces caspase-3-mediated apoptosis in promyelocytic leukemia HL-60 cells[4].
Sargachromanol E inhibits long-wave ultraviolet-induced senescence in human skin fibroblasts[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:human promyelocytic leukemia HL-60 cells
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Concentration:12.5, 25, 50 μM
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Incubation Time:24 h
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Result:Induced dose-dependent nuclear morphological changes characteristic of apoptosis.\n
Induced the characteristic DNA laddering pattern indicative of apoptotic DNA fragmentation in treated cells.
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Cell Line:human promyelocytic leukemia HL-60 cells
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Concentration:12.5, 25, 50 μM
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Incubation Time:24 h
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Result:Caused concentration-dependent increases in sub-G1 hypodiploid cells.
Showed no mitotic block or delay in G2/M phase.
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Cell Line:human promyelocytic leukemia HL-60 cells
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Concentration:12.5, 25 μM
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Incubation Time:24 h
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Result:Caused a slight increase in pro-apoptotic Bax protein levels, a marked decrease in anti-apoptotic Bcl-xL protein levels, an increase in active cleaved caspase-3 levels, a decrease in pro-caspase-9 levels, and cleavage of PARP, with these effects most pronounced at 25 μM.
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Cell Line:RAW 264.7 murine macrophages
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Concentration:5, 12.5, 25 μg/mL
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Incubation Time:2 h pretreatment
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Result:Dose-dependently reduced LPS-stimulated PGE2 production.
Significantly decreased PGE2 levels at 5 μg/mL.
Caused a greater reduction of PGE2 production at 12.5 μg/mL.
Reduced PGE2 production to ~20% of LPS-only treated cells at 25 μg/mL.\nDose-dependently reduced LPS-stimulated TNF-α and IL-1β production.
Significantly reduced TNF-α production at 5 μg/mL, with further decreases to ~50% of LPS-only levels at 12.5 μg/mL and 25 μg/mL.
Significantly reduced IL-1β production at 5 μg/mL and 12.5 μg/mL, and nearly completely inhibited it at 25 μg/mL.
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Cell Line:RAW 264.7 murine macrophages
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Concentration:5, 12.5, 25 μg/mL
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Incubation Time:2 h pretreatment
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Result:Dose-dependently suppressed LPS-stimulated COX-2 and iNOS protein expression.
Nearly completely inhibited COX-2 expression at 12.5 μg/mL and 25 μg/mL.
Significantly reduced iNOS expression at 5 μg/mL, with further dose-dependent decreases at 12.5 μg/mL and 25 μg/mL.
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Cell Line:RAW 264.7 murine macrophages
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Concentration:5, 12.5, 25 μg/mL
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Incubation Time:2 h pretreatment
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Result:Dose-dependently suppressed LPS-stimulated phosphorylation of ERK1/2 and JNK, and slightly reduced phosphorylation of p38.
Significantly reduced ERK1/2 phosphorylation at 5 μg/mL, with further decreases at 12.5 μg/mL and 25 μg/mL.
Strongly inhibited JNK phosphorylation at all tested concentrations, with near-complete inhibition at 25 μg/mL.
Showed a moderate, dose-dependent reduction of p38 phosphorylation.
Chemical Information
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CAS No. 856414-54-5
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분자량 428.60
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화학식 C27H40O4
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SMILES
C/C(C)=C\[C@@H]([C@H](/C(C)=C/CC/C(C)=C/CC[C@@]1(CCC2=CC(O)=CC(C)=C2O1)C)O)O
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Structure Classification
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Initial Source
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
순도&문서
References
[1]. Heo SJ, et al. Chromene induces apoptosis via caspase-3 activation in human leukemia HL-60 cells. Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association. 2011 Sep;49(9):1998-2004. [Content Brief]
[2]. Lee JH, et al. Preparative isolation of sargachromanol E from Sargassum siliquastrum by centrifugal partition chromatography and its anti-inflammatory activity. Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association. 2013 Dec;62:54-60. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Sargachromanol E Related Classifications
HY-123364 Related Classifications
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