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【bio-news】科学家发现血清素再吸收抑制剂与骨质
Contact: Jennifer Kelly
jkelly@forsyth.org
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Forsyth Institute
Forsyth scientists find linkages between serotonin reuptake inhibitors and bone mass
Commonly used antidepressants may prevent bone loss
Boston-- Scientists at The Forsyth Institute have found that fluoxetine (Prozac), a drug used in the treatment of depression and obsessive-compulsive disorders, increases bone mass. The team of researchers analyzed the ability of fluoxetine to stimulate new bone formation under normal conditions and to block bone loss caused by inflammation or estrogen loss due to ovariectomy. They found that the antidepressant induced the formation of new bone under normal conditions and reversed total bone loss triggered by inflammation.
Bone destruction is characteristic of several chronic inflammatory diseases including rheumatoid arthritis and gum disease. Previous research has shown a correlation between the serotonin transporter -- serotonin is the chemical substance involved in transmitting signals between neurons and which plays a role in anxiety and mood disorders-- and bone destructive cells (osteoclasts). (Fluoxetine is a serotonin reuptake inhibitor (SSRIs).) However, it was not clear what role serotonin played in bone metabolism.
Summary of Study
Trabecular bone, one of two main types of bone, is spongy, and makes up the bulk of the interior of most bones, including the vertebrae. After a six-week treatment with fluoxetine, laboratory mice showed increased trabecular bone volume and total volume in femurs and vertebrae as determined by micro-computed tomography. Fluoxetine-treated animals were not protected from bone loss after ovariectomy, suggesting that its anabolic effect requires the presence of estrogen. The effect on bone loss was also investigated following a bacterial-mediated inflammatory challenge. Injections of lipopolysaccharide (LPS), a component of the membrane of certain strains of bacteria, resulted in an increased number of osteoclasts and net bone loss. However, LPS given with fluoxetine caused new bone formation and a net gain in bone mass. The study concluded that fluoxetine treatment in vivo leads to increased bone mass under normal physiological conditions or inflammatory conditions, but does not prevent bone loss associated with estrogen deficiency.
This research, which will be published in the next issue of the Journal of Cellular Biochemistry, currently available online, was led by Ricardo Battaglino, PhD, Assistant Member of the Staff in the Department of Cytokine Biology at The Forsyth Institute.
"As this class of medication is widely prescribed and used across all age groups, the consequences of the relationship between these drugs and bone metabolism may be very relevant to public health. This work will help us learn more about the underlying causes of osteoporosis and gain a new understanding of bone formation at a molecular level," said Dr. Battaglino. "Furthermore, this research provides exciting clues on how to prevent destructive bone loss and even improve bone mass in certain medical/dental conditions."
http://www.eurekalert.org/bysubject/biology.php 认领了!谢谢! 科学家发现5-羟色胺再吸收抑制剂与骨量相关--常用的抗抑郁症药物时可能会防止骨质丢失
波士顿----Forsyth研究所的一些科学家发现一种治疗抑郁症、强迫症的药物氟西汀（又称百忧解）可以使骨量增加。研究人员们分析了氟西汀在正常情况刺激新骨生成的能力，同时还分析了它对炎症或卵巢切除术后雌激素水平降低所产生的骨丢失的抑制作用。结果发现这种抗抑郁症药物能在正常状态下诱导新骨形成，并且抑制了炎症导致的总骨量丢失。
骨组织破坏是一些慢性炎性疾病包括类风湿性关节炎和齿龈疾病的特性。之前的研究已经表明5-羟色胺转运体（5-羟色胺是一种可在神经元之间传递信号的化学物质，它还在焦虑和情绪紊乱中扮有重要角色）和破骨细胞有关。氟西汀是一种5-羟色胺再吸收的抑制剂（SSRIs）.然而，血清素在骨代谢中具体起什么作用，并不清楚。
研究概要
骨小梁，即骨松质（骨组织两种重要类型中的一类），是包括椎骨在内的大多数骨骼内部结构的重要组成。在使用氟西汀治疗6个星期后，显微ＣＴ检测到实验鼠的股骨和椎骨内骨小梁的量和总骨量都有增加。但是做了卵巢切除术后再接受氟西汀治疗的实验动物，骨丢失的现象并没有被抑制，这也暗示，氟西汀促进骨形成的合成代谢效应需要雌激素的参与。细菌介导的炎症同样被证实可以引起骨丢失。因而，向实验动物注射脂多糖（（LPS）某些细菌细胞膜上的成分）后导致破骨细胞数量增加，骨梁网丢失。然而，在给予LPS的同时向动物注射氟西汀后却使新骨形成，骨质内获得新的骨梁网。因而，可以推断在正常生理状态或者炎症时使用氟西汀体内治疗可以使骨量增加，但是，氟西汀并不能防治雌激素缺乏所致的骨丢失。
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作者:admin@医学,生命科学 2010-11-22 05:11
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