γ-Elemene
γ-Elemene ((-)-γ-Elemene) is a lipid-lowering agent. γ-Elemene increases superoxide dismutase (SOD). γ-Elemene reduces the expression of adhesion molecules (VCAM-1, ICAM-1) in cells damaged by H2O2. γ-Elemene regulates lipid peroxidation. γ-Elemene protects cells from peroxidative damage induced by high fat and H2O2. γ-Elemene decreases lipid content. γ-Elemene can be used in the research of atherosclerosis.
For research use only. We do not sell to patients.
- CAS No.: 29873-99-2
- Formula: C15H24
- Molecular Weight:204.36
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Storage:
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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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
In Vitro
γ-Elemene and (-)-γ-Elemene (1 μg/mL; 24 h) exert antioxidant protective effects against H2O2-induced oxidative damage in human umbilical vein endothelial cells (HUVEC). The increase rates of superoxide dismutase (SOD) induced by them are 23.75% and 22.45%, respectively, while the decrease rates of malondialdehyde (MDA) are 35.22% and 36.82%, respectively[1].
(-)-γ-Elemene (24 h) reduces the expression of adhesion factors in H2O2-injured HUVEC cells, with a reduction rate of 22.87% for VCAM-1 and 15.58% for ICAM-1[1].
(-)-γ-Elemene (24 h) reduces intracellular lipid levels in free fatty acid (FFA)-loaded HepG2 cells, with a triglyceride (TG) reduction rate of 21.39% and a non-esterified fatty acid (NEFA) reduction rate of 16.43%[1].
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:human umbilical vein endothelial cells (HUVEC)
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Concentration:Not specified
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Incubation Time:24 h
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Result:Reduced ICAM-1 levels by 15.58%.
Reduced VCAM-1 levels by 22.87%.
Chemical Information
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CAS No. 29873-99-2
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Molecular Weight 204.36
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Formula C15H24
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SMILES
C(C)(=C)[C@@H]1[C@](C=C)(C)CCC(=C(C)C)C1
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Synonyms
(-)-γ-Elemene
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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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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
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Ferroptosis Solutions
Ferroptosis is an iron-dependent, non-apoptotic form of regulated cell death characterized by lethal lipid peroxidation and sensitivity to suppression by iron chelators or lipophilic radical-trapping antioxidants. The core pathway links cystine uptake through system Xc−, glutathione availability, GPX4-dependent detoxification of phospholipid hydroperoxides, iron-dependent oxidative reactions, and polyunsaturated-phospholipid metabolism into a cell-death program that is biochemically and morphologically distinct from apoptosis, necrosis, and autophagy. The ferroptosis pathway is experimentally linked to phenotype through chemical and genetic perturbation. Erastin induces ferroptosis by inhibiting cystine uptake through system Xc− and weakening antioxidant defenses, while GPX4 inhibition or depletion causes lipid peroxide accumulation and ferroptotic cancer-cell death. ACSL4 and oxidizable arachidonoyl- or adrenoyl-containing phosphatidylethanolamines shape ferroptosis sensitivity by con
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
γ-Elemene Related Classifications
HY-135876 Related Classifications
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