首页> 外文会议>Annual Meeting of the Japanese Association for Animal Cell Technology >PHVTOESTROGENS ENHANCE THE ACETYLCHOLINESTERASE ACTIVITY OF THE RAT PHEOCHROMOCYTOMA CELL LINE PC12 BY BINDING TO THE ESTROGEN RECEPTOR
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PHVTOESTROGENS ENHANCE THE ACETYLCHOLINESTERASE ACTIVITY OF THE RAT PHEOCHROMOCYTOMA CELL LINE PC12 BY BINDING TO THE ESTROGEN RECEPTOR

机译:通过与雌激素受体结合来增强大鼠嗜铬细胞瘤细胞系PC12的乙酰胆碱酯酶活性

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Some compounds derived from plants have been known to possess estrogenic properties and can thus alter the physiology of higher organisms. Genistein and daidzin are examples of these phytoestrogens, which have recently been the subject of extensive research. In this study, genistein and daidzin were found to enhance the acetylcholinesterase (AChE) activity of the rat neuronal ceU line PC12 at concentrations as low as 0.08 μM by binding to the estrogen receptor (ER). Results have shown that this enhancement was effectively blocked by the known estrogen receptor antagonist tamosifen, indicating the involvement of the ER in AChE induction. On the other hand, incubating the PC12 cells in increasing concentrations of 17 6-estradiol (E2) did not lead toenhanced AChE activity, even in the presence of genistein or daidzin. This suggests that mere binding of an estrogenic compound to the ER does not necessarily lead to enhanced AChE activity. Moreover, the effect of the phytoestrogens on AChE activity cannot be expressed in the presence of E2 since they either could not compete with the natural ligand in binding to the ER or that E2 down-regulates its own receptor. This study clearly suggests that genistein and daidzin enhance AChE activity in PC12 cells by binding to the ER; however, the actual mechanism of enhancement is not known.
机译:已知一些源自植物的化合物具有雌激素性质,因此可以改变更高生物的生理学。 Genistein和Daidzin是这些植物雌激素的实例,最近是广泛研究的主题。在该研究中,发现Genistein和Daidzin通过与雌激素受体(ER)结合,以低至0.08μm的浓度为低至0.08μm的乙酰胆碱酯酶(疼痛)活性。结果表明,已知的雌激素受体拮抗剂Tamosifen有效地阻断了这种增强,表明ER在疼痛诱导中的累积。另一方面,即使在Genistein或Daidzin的存在下,孵育在17 6-雌二醇(E2)的浓度增加中的浓度增加并未导致疼痛的疼痛活性。这表明仅仅是雌激素化合物与ER的结合并不一定导致增强的疼痛活性。此外,植物雌激素对疼痛活性的影响不能在E2的存在下表达,因为它们不能与天然配体竞争结合ER或E2下调其自己的受体。本研究清楚地表明,Genistein和Daidzin通过与ER结合来增强PC12细胞中的疼痛活性;然而,增强的实际机制是不知道的。

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