Dehydrotrametenolic acid
產(chǎn)品名稱(chēng):Dehydrotrametenolic acid
產(chǎn)品描述:
植物來(lái)源 | 天然產(chǎn)物 > 多孔菌科 > 茯苓屬 |
結(jié)構(gòu)類(lèi)型 | 天然產(chǎn)物 > 萜類(lèi) |
產(chǎn)品描述 | Dehydroeburicoic acid induces necrotic cell death that involves Ca(2+) overload, mitochondrial dysfunction, and calpain activation in human glioblastomas. |
體外活性 | 3-(4,5-Dimethyl-thiazol-2-yl)-2,5-diphenyltetrazolium bromide and lactate dehydrogenase release assays indicated that Dehydroeburicoic acid inhibited the proliferation of the human glioblastoma cell U87MG. In addition, Annexin V and propidium iodide staining showed that Dehydroeburicoic acid treatment led to a rapid increase of glioblastomas in the necrotic/late apoptotic fraction, whereas cell cycle analysis revealed that Dehydroeburicoic acid failed to significantly enhance the population of U87MG cells in the hypodiploid (sub-G1) fraction. Using electron microscopy, we found that Dehydroeburicoic acid induced significant cell enlargements, massive cytoplasmic vacuolization, and loss of mitochondrial membrane integrity. Dehydroeburicoic acid treatment triggered an intracellular Ca(2+) increase, and Dehydroeburicoic acid-induced cell death was significantly attenuated by BAPTA-AM but not ethylenediaminetetraacetic acid or ethylene glycol tetraacetic acid. Dehydroeburicoic acid instigated a reduction of both mitochondrial transmembrane potential and intracellular ATP level. Moreover, Dehydroeburicoic acid induced proteolysis of alpha-spectrin by calpain, and Dehydroeburicoic acid cytotoxicity in U87MG cells was caspase-independent but was effectively blocked by calpain inhibitor. Interestingly, Dehydroeburicoic acid also caused autophagic response that was prevented by calpain inhibitor. |
別名 | 去氫齒孔酸, Dehydroeburicoic acid, 松苓新酸 |
分子量 | 468.73 |
分子式 | C3lH48O3 |
CAS No. | 6879-05-6 |
存儲(chǔ)
Powder: -20°C for 3 years | In solvent: -80°C for 2 years
溶解度
DMSO: 10 mM
( < 1 mg/mL refers to the product slightly soluble or insoluble )
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