β-Estradiol

Estradiol is a steroid sex hormone vital to the maintenance of fertility and secondary sexual characteristics in females. Estradiol upregulates IL-6 expression through the estrogen receptor β (ERβ) pathway.

＞98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

雌二醇; β-Estradiol; E2; 17β-Estradiol; 17β-Oestradiol

White to off-white powder

DMSO : ≥ 50 mg/mL (183.57 mM)
Ethanol : 20 mg/mL (73.43 mM; Need ultrasonic)

Estrogen receptor

Estradiol induces new dendritic spines and synapses on hippocampal CA1 pyramidal cells. Estradiol treatment resulted in a 46% increase in NMDA receptor binding. Estradiol treatment increases NMDA receptor binding in parallel with dendritic spine and synapse density. Estradiol treatment results in increased sensitivity of CA1 pyramidal cells to NMDA receptor-mediated synaptic input and that this increase is well correlated with the estradiol-induced increase in dendritic spine density in the apical dendritic tree of these cells. 17 beta-estradiol is found to reduce Ba2+ entry reversibly via Ca2+ channels in acutely dissociated and cultured neostriatal neurons. 17 alpha-Estradiol also reduces Ba2+ currents but is significantly less effective than 17 beta-estradiol in rat neostriatal neurons. 17 beta-estradiol exerts a dose-dependent inhibition of IL-1-, TNF-, and IL-1 and TNF-induced production of bioassayable IL-6. Estradiol inhibits both TNF-induced IL-6 production and osteoclast development in primary bone cell cultures derived from neonatal murine calvaria.

Estradiol mediates fluctuation in hippocampal synapse density during the estrous cycle in the adult rat. Estradiol alone can reverse the ovariectomy-induced decrease in spine density. Estradiol combined with Progesterone initially increases spine density for a period of 2 to 6 hours but then results in a much sharper decrease than is observed following estradiol alone.