雌二醇

beta-Estradiol

	产品编号	CFN90035
	CAS编号	50-28-2
	分子式 = 分子量	C₁₈H₂₄O₂ = 272.38
	产品纯度	>=98%
	物理属性	Powder
	化合物类型	Steroids
	植物来源
ChemFaces的产品在影响因子大于5的优秀和顶级科学期刊中被引用

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产品名称	产品编号	CAS编号	包装	QQ客服
雌二醇	CFN90035	50-28-2	10mg	QQ客服：1457312923
雌二醇	CFN90035	50-28-2	20mg	QQ客服：1457312923
雌二醇	CFN90035	50-28-2	50mg	QQ客服：1457312923
雌二醇	CFN90035	50-28-2	100mg	QQ客服：1457312923

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Description:

Estradiol, or more precisely, 17β-estradiol, is a human sex hormone and steroid, and the primary female sex hormone. Beta-estradiol has been considered to be a neurotrophic agent, beta-estradiol at a dose of 0.25 microg/day prevents ischemia-induced learning disability and neuronal loss at early stages after transient forebrain ischemia, possibly via a receptor-mediated pathway without attenuating free radical neurotoxicity.

Targets:

LDL

In vitro:

FEBS J. 2015 Jul;282(14):2682-96.

β-Estradiol results in a proprotein convertase subtilisin/kexin type 9-dependent increase in low-density lipoprotein receptor levels in human hepatic HuH7 cells.[Pubmed: 25913303]

The lower risk of coronary artery disease in premenopausal women than in men and postmenopausal women implicates sex steroids in cardioprotective processes. beta-Estradiol upregulates liver low-density lipoprotein receptor (LDLR), which, in turn, decreases circulating levels of low-density lipoprotein, which is a risk factor for coronary artery disease. Conversely, LDLR protein is negatively regulated by proprotein convertase subtilisin/kexin type 9 (PCSK9).
METHODS AND RESULTS:
Herein, we investigated PCSK9 regulation by beta-Estradiol and its impact on LDLR in human hepatocarcinoma HuH7 cells grown in the presence or absence of β-estradiol. Immunoblot analysis showed upregulation of LDLR at 3 μm beta-Estradiol (140%), and the upregulation reached 220% at 10 μm beta-Estradiol; only at the latter dose was an increase in LDLR mRNA detected by qPCR, suggesting post-translational regulation of LDLR. No changes in PCSK9 mRNA or secreted protein levels were detected by qPCR or ELISA, respectively. beta-Estradiol-conditioned medium devoid of PCSK9 failed to upregulate LDLR. Similarly, PCSK9 knockdown cells showed no upregulation of LDLR by beta-Estradiol. Together, these results indicate a requirement for PCSK9 in the beta-Estradiol-induced upregulation of LDLR. A radiolabeling assay showed a significant, dose-dependent decrease in the ratio of secreted phosphoPCSK9 to total secreted PCSK9 with increasing beta-Estradiol levels, suggesting a change in the functional state of PCSK9 in the presence of beta-Estradiol.
CONCLUSIONS:
Our results indicate that the protein upregulation of LDLR at subtranscriptionally effective doses of beta-Estradiol, and its supratranscriptional upregulation at 10 μm beta-Estradiol, occur through an extracellular PCSK9-dependent mechanism.

In vivo:

Epilepsy Res. 2013 Dec;107(3):297-301.

Gonadal status-dependent effects of in vivo β-estradiol administration to female rats on in vitro epileptiform activity induced by low [Mg2+]₀ in combined hippocampus-entorhinal cortex slices.[Pubmed: 24113171]

There are controversial data regarding estrogen effects on neuronal excitability.
METHODS AND RESULTS:
We investigated whether beta-Estradiol (EB) administration to ovariectomized (OVX) or gonadally intact female rats alters epileptiform activity within the dentate gyrus network induced in vitro by removing [Mg2+]o in combined hippocampus-entorhinal cortex slices. In vivo beta-Estradiol administration significantly influenced the epileptiform activity in gonadal status-dependent manner. The onset of epileptiform discharges was modestly delayed in slices from OVX rats replaced with physiologically relevant doses of beta-Estradiol but the number of discharges was not affected. In contrast, beta-Estradiol administration to gonadally intact rats had robust effects such that: beta-Estradiol delayed the onset of discharges but significantly increased their number within the dentate gyrus network.
CONCLUSIONS:
Our data suggest that beta-Estradiol in physiologically relevant concentrations does not seem to negatively affect hippocampal neuronal excitability, nevertheless supraphysiological beta-Estradiol levels may enhance seizure severity.

	1 mg	5 mg	10 mg	20 mg	25 mg
1 mM	3.6713 mL	18.3567 mL	36.7134 mL	73.4268 mL	91.7835 mL
5 mM	0.7343 mL	3.6713 mL	7.3427 mL	14.6854 mL	18.3567 mL
10 mM	0.3671 mL	1.8357 mL	3.6713 mL	7.3427 mL	9.1784 mL
50 mM	0.0734 mL	0.3671 mL	0.7343 mL	1.4685 mL	1.8357 mL
100 mM	0.0367 mL	0.1836 mL	0.3671 mL	0.7343 mL	0.9178 mL

产品名称	产品编号	CAS编号	分子式 = 分子量	位单	联系QQ
红苋甾酮; Rubrosterone	CFN90840	19466-41-2	C₁₉H₂₆O₅ = 334.4	5mg	QQ客服：215959384
去氢表雄酮; Dehydroepiandrosterone	CFN90043	53-43-0	C₁₉H₂₈O₂ = 288.42	20mg	QQ客服：215959384
睾酮; Testosterone	CFN90034	58-22-0	C₁₉H₂₈O₂ = 288.42	20mg	QQ客服：1413575084
雌二醇; beta-Estradiol	CFN90035	50-28-2	C₁₈H₂₄O₂ = 272.38	20mg	QQ客服：2159513211
17α-雌二醇; 17alpha-Estradiol	CFN96786	57-91-0	C₁₈H₂₄O₂ = 272.38	5mg	QQ客服：1413575084
雌酚酮; Estrone	CFN90042	53-16-7	C₁₈H₂₂O₂ = 270.37	20mg	QQ客服：1413575084
固甾酮; Guggulsterone E&Z	CFN93007	95975-55-6	C₂₁H₂₈O₂ = 312.5	5mg	QQ客服：2056216494

雌二醇

beta-Estradiol

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