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首页> 外文期刊>The European Journal of Neuroscience >Nicotine reduces A beta in the brain and cerebral vessels of APPsw mice.
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Nicotine reduces A beta in the brain and cerebral vessels of APPsw mice.

机译:尼古丁会降低APPsw小鼠大脑和脑血管中的A beta。

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摘要

Ten days treatment with nicotine reduced insoluble amyloid A beta 1-40 and Alpha beta 1-42 peptides by 80% in the cortex of 9-month-old APPsw mice, which is more than that observed in 14.5-month-old mice following nicotine treatment for 5.5 months. A reduction in A beta associated with cerebral vessels was observed in addition to that deposited as parenchymal plaques after 5.5 months treatment. The diminution in A beta peptides observed was not accompanied by changes in brain alpha, beta or gamma secretase-like activities, NGF or BDNF protein expression measured in brain homogenates. A significant increase in sAPP was observed after nicotine treatment of SH-SY5Yneuroblastoma cells that could be blocked by the nicotinic antagonist mecamylamine. Attenuation of elevated [(125)I]-alpha bungarotoxin binding (alpha 7) in APPsw mice was observed after 5.5 months nicotine treatment. Both these observations suggest that the reduction in insoluble A beta by nicotine might be in part mediated via the alpha 7 nicotinic receptor. Further studies are required to identify potential mechanisms of the nicotine's amyloid-reducing effect.
机译:尼古丁治疗10天后,在9个月大的APPsw小鼠的皮层中将不溶性淀粉样蛋白A beta 1-40和Alpha beta 1-42肽减少了80%,这比在接受尼古丁治疗的14.5个月大小鼠中观察到的要多。治疗5.5个月。在5.5个月的治疗后,除了沉积为实质性斑块的沉积物外,还观察到与脑血管相关的Aβ含量降低。观察到的Aβ肽减少并没有伴随脑α,β或γ分泌酶样活性,脑匀浆中NGF或BDNF蛋白表达的变化。尼古丁处理SH-SY5Y母细胞瘤细胞后,sAPP显着增加,这可能被烟碱类拮抗剂美卡明胺所阻断。尼古丁治疗5.5个月后,在APPsw小鼠中观察到[[125)I]-αBungarotoxin结合(α7)升高的减弱。这两个发现都表明尼古丁对不溶性Aβ的减少可能部分是通过α7烟碱受体介导的。需要进一步的研究来确定尼古丁的淀粉样蛋白减少作用的潜在机制。

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