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【drug-news】炎症可诱发阿尔海默兹症

最后编辑于 2022-10-09 · IP 江苏江苏
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这个帖子发布于 15 年零 355 天前,其中的信息可能已发生改变或有所发展。
http://www.sciencedaily.com/releases/2009/07/090708181204.htm

Inflammation May Trigger Alzheimer's Disease
炎症可诱发阿尔海默兹症
ScienceDaily (July 8, 2009) — The anti-inflammatory drug indomethacin could hold promise as a treatment for Alzheimer's disease, says a Saint Louis University doctor and researcher.
ScienceDaily (July 8, 2009) —圣路易斯大学的研究人员称,抗炎药物—吲哚美辛具有治疗阿尔海默症的作用。
Two research studies published by William A. Banks, M.D., professor of geriatrics and pharmacological and physiological science at Saint Louis University School of Medicine, support this conclusion and offer what he calls a "one-two punch" in giving clues on how Alzheimer's disease develops and could be treated.
美国圣路易斯大学医学院的老年医学、药理学和生理学的教授William A. Banks博士发表的两份研究报告支持了这一结论,并提出其所说的“联合效应”能解释阿尔茨海默氏症如何发展和治疗。
His study in the July edition of the Journal of Alzheimer's Disease supports the idea that toxic levels of amyloid beta protein, the substance scientists believe is responsible for Alzheimer's disease, accumulate in the brain because a pump that pushes it into the blood and past the blood-brain barrier malfunctions.
在7月出版的阿尔海默兹症杂志中,他的研究支持β-淀粉样蛋白的毒性观点,科学家认为该物质是诱导阿尔茨海默症的重要因素。通过一个泵,该物质被泵入血液并穿过功能受损的血脑屏障,在大脑中沉积。
The blood-brain barrier is a system of cells that regulates the exchange of substances between the brain and the blood. The blood-brain barrier transporter known as LRP is the pump that removes amyloid beta protein from the brain and into the bloodstream. 血脑屏障是一个细胞系统,它能调节大脑和血液间的物质交换。众所周知的血脑屏障转运体—LRP是一个能将β-淀粉样蛋白从大脑中外排和进入血液的转运泵。
"LRP malfunctions like a stop light stuck on red, and keeps amyloid beta protein trapped in the brain," said Banks, who also is a staff physician at Veterans Affairs Medical Center in St. Louis.
“正如交通灯停留在红灯一样,LRP的表达故障能使β-淀粉样蛋白残留在大脑中。”圣路易斯的退伍军人医疗中心的医师Banks说。
He tested the hypothesis by giving mice an antisense, which is a molecular compound that blocked the production of LRP. Amyloid beta protein accumulated in the brain and the mice showed memory loss and learning impairment.
他给小鼠服用反意物质—一种阻碍LRP表达的分子化合物—用来验证自己的猜想。β-淀粉样蛋白在大脑中积累和小鼠表现出记忆丧失和学习障碍。
The finding raises the question of what causes LRP to malfunction. Banks' study in the May issue of Brain Behavior and Immunity suggests inflammation as the culprit and supports using indomethacin, an anti-inflammatory medication, as a buffer to protect LRP from being turned off.
这一发现提出了一个问题:是什么原因导致LRP功能障碍。在5月版的大脑行为与免疫发表的Banks的研究暗示炎症是罪魁祸首,并指出消炎药物—吲哚美辛—可作为预防LRP关闭的保护剂。
Inflammation, which is part of the body's natural immune response, occurs when the body activates white blood cells and produces chemicals to fight infection and invading foreign substances.
为对抗感染和外来物质的侵入,人体激活白细胞和生产化学因子时,人体自然免疫反应的组成部分—炎症反应就发生了。
"We induced inflammation in mice and found that it turned off the LRP pump that lets amyloid beta protein exit the brain into the bloodstream. It also revved up an entrance pump that transports amyloid beta into the brain. Both of these actions would increase the amount of amyloid beta protein in the brain."
“利用小鼠,我们诱导炎症反应并发现炎症能将β-淀粉样蛋白从大脑排入血液的LRP泵关闭了。炎症还能开放一个将β-淀粉样蛋白运输到大脑中的输入泵。这两个作用将增加β-淀粉样蛋白在大脑中的沉积。”
Banks then gave mice indomethacin, which prevented inflammation from turning off the LRP (exit pump).
然后Banks给小鼠服用吲哚美辛—通过关闭LRP(外排泵)抑制炎症。
His findings help to explain what doctors who are studying the use of indomethacin to treat people with Alzheimer's disease are seeing in their clinical practice.
对于那些研究吲哚美辛在阿尔茨海默氏症患者治疗中用途的医生,他的研究结果可帮助他们理解他们在临床实践所看到的现象。
"Nonsteroidal anti-inflammatory drugs, especially indomethacin, have been associated with protection against Alzheimer's disease. Our work could influence that debate and thinking at the patient-care level," Banks said.
班克斯说:“非甾体抗炎药—特别是吲哚美辛—已证明有助于老年痴呆症的预防。我们的工作将影响患者治疗水平方面的争论和思考”。

























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