Immobilization stress-induced anorexia is mediated independent of MyD88.
Immobilization stress-induced anorexia is mediated independent of MyD88.
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固定应激诱导的厌食症是独立于 MyD88 介导的。
DOI：
10.1097/wnr.0000000000000641
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发表时间：
2016
期刊：
影响因子：
1.7
通讯作者：
Ozawa K
中科院分区：
文献类型：
--
作者：
Hosoi T;Yamawaki Y;Kimura H;Ozawa K
MyD88是Toll样受体的衔接蛋白，其参与调节先天免疫功能。脂多糖诱导的Toll样受体4信号转导激活通过MyD88诱导下丘脑信号转导和转录激活因子3（STAT3）磷酸化和厌食症。在本研究中，我们调查了MyD88在心理应激诱发的厌食症中的可能作用。我们发现固定应激抑制了野生型小鼠和MyD88缺陷小鼠的食物摄入。固定应激轻微增加了下丘脑中的STAT3磷酸化，但它弱于脂多糖诱导的STAT3磷酸化的增加。这些观察结果表明，心理压力引起的厌食症的机制可能是调节不同的厌食症，是由感染引起的。
MyD88 is an adaptor protein for the toll-like receptor, which is involved in regulating innate immune function. Lipopolysaccharide-induced activation of toll-like receptor 4 signaling induces hypothalamic signal transducer and activator of transcription 3 (STAT3) phosphorylation and anorexia through MyD88. In the present study, we investigated the possible role of MyD88 in psychological stress-induced anorexia. We found that immobilization stress inhibited food intake in both wild-type mice and MyD88-deficient mice. Immobilization stress slightly increased STAT3 phosphorylation in the hypothalamus, but it was weaker than the lipopolysaccharide-induced increase in STAT3 phosphorylation. These observations suggest that the mechanisms involved in psychological stress-induced anorexia may be regulated differently from those involved in anorexia that is induced by infection.