The role of brain-derived neurotrophic factor in experimental inflammation of mouse gut
The role of brain-derived neurotrophic factor in experimental inflammation of mouse gut
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脑源性神经营养因子在小鼠肠道实验性炎症中的作用
DOI：
10.1016/j.ejpain.2009.10.007
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发表时间：
2010-07-01
影响因子：
3.6
通讯作者：
Li, Yanqing
中科院分区：
文献类型：
--
作者：
Yang, Jing;Yu, Yanbo;Li, Yanqing
以往的研究表明，脑源性神经营养因子(BDNF)可能是慢性疼痛状态的重要调节剂。然而，还没有系统的研究使用基因敲除小鼠来阐明其对内脏敏感性的影响。本研究用2，4，6-三硝基苯磺酸(TNBS)诱导杂合子(BDNF+/)和野生型(BDNF+/+)小鼠结肠炎。记录结肠扩张(CRD)时的内脏反应和膀胱的反应性。结果表明，在正常状态下，BDNF+/和BDNF+/+小鼠对CRD的内脏反应在=60 mm Hg压力下没有差异，BDNF+/小鼠对CRD的内脏反应较弱。在炎症性结肠炎状态下，TNBS可诱导两种基因型小鼠背根神经节BDNF表达上调，而BDNF+/小鼠在30 mm Hg时对结肠和膀胱的敏感性均显著低于BDNF+/+小鼠。两种基因型在炎症严重程度上没有显著差异。因此，BDNF缺乏会导致对照组和炎症状态下结肠伤害性感觉的发育变化，其中炎症状态下的变化更为显著。对于膀胱的反应性，BDNF缺乏导致炎症状态下较低的敏感度，但在对照状态下没有影响。观点：本文强调了BDNF在小鼠结肠和牵涉膀胱痛过敏中的作用。这些发现可能有助于确定针对BDNF的缓解腹痛的新药物干预措施。(C)2009年欧洲国际疼痛研究协会联合会。爱思唯尔有限公司出版。保留所有权利。
Previous studies suggested that brain-derived neurotrophic factor (BDNF) might act as an important modulator in chronic pain states. However, no systematic study has used knock-out mice to clarify its effect on visceral sensitivity. In the present study, 2,4,6-trinitrobenzene sulfonic acid (TNBS) was administered to heterozygous (BDNF+/ ) knock-out and wild-type (BDNF+/+) mice to induce colitis. Visceral response to colorectal distension (CRD) and bladder reactivity were recorded. Results demonstrated that in normal state, BDNF+/ and BDNF+/+ mice did not differ in the visceral response to CRD at = 60 mm Hg pressure, BDNF+/ mice showed a weaker visceral response to CRD. In inflammatory state of colitis, TNBS induced upregulation of BDNF in dorsal root ganglia of both genotypes while BDNF+/ mice showing significantly lower sensitivity in the colon at >= 30 mm Hg and lower sensitivity in bladder than BDNF+/+ mice. The two genotypes showed no significant difference in inflammatory severity. Thus, BDNF deficiency results in developmental changes in colonic nociception in both control and inflammatory states, which are more significant in inflammatory state. For bladder reactivity, BDNF deficiency leads to lower sensitization in inflammatory state but has no effect in control state.Perspective: This article highlights the role of BDNF in colonic and referred bladder hyperalgesia in mice. The findings might help in determining novel pharmaceutical interventions targeted at BDNF to relieve abdominal pain. (C) 2009 European Federation of International Association for the Study of Pain Chapters. Published by Elsevier Ltd. All rights reserved.