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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Lipopolysaccharide (LPS) stimulates adipokine and socs3 gene expression in mouse brain and pituitary gland in vivo, and in N-1 hypothalamic neurons in vitro.
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Lipopolysaccharide (LPS) stimulates adipokine and socs3 gene expression in mouse brain and pituitary gland in vivo, and in N-1 hypothalamic neurons in vitro.

机译：脂多糖（LPS）在体内和体外N-1下丘脑神经元中刺激脂肪因子和socs3基因表达。

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Adipokines that modulate metabolic and inflammatory responses, such as resistin (rstn) and fasting-induced adipose factor (fiaf), are also expressed in mouse brain and pituitary gland. Since lipopolysaccharide (LPS)-induced endotoxinemia provokes an anorectic response via a hypothalamic-dependent mechanism we hypothesized that LPS would also modify hypothalamic adipokine expression. Challenging male CD-1 mice with LPS (5 mg/kg; s.c.) significantly reduced bodyweight (24 h) and realtime RT-PCR revealed time- and tissue-dependent increases in rstn, fiaf and suppressor of cytokine signaling-3 (socs-3) mRNA in hypothalamic, pituitary, cortical and adipose tissues. Gene expression was rapidly increased (3-6 h) in the hypothalamus and pituitary, but returned to normal within 24 h. In contrast, with the exception of rstn in fat, the expression of target genes remained elevated in cortex and visceral fat at 24 h post-injection. In order to more specifically examine the hypothalamic response to LPS we investigated its effects directly on N-1 hypothalamic neurons in vitro. LPS (25 microg/mL; 3 h) had no effect on rstn mRNA, but significantly stimulated fiaf and socs-3 expression. Although various toll-like receptor 4 (TLR4) antagonists (parthenolide, PD098059, and SB202190) did not prevent the LPS-induced increases in fiaf and socs-3, they did partially attenuate its stimulatory effects. We conclude that LPS treatment increases the expression of central, and possibly neuronal, adipokine genes which may influence local tissue repair and function, but could also have downstream consequences on the hypothalamic control of appetite and energy metabolism following an inflammatory insult.
机译：调节代谢和炎症反应的脂肪因子，例如抵抗素（rstn）和空腹诱导的脂肪因子（fiaf），也在小鼠大脑和垂体中表达。由于脂多糖（LPS）诱导的内毒素血症通过下丘脑依赖性机制引起厌食反应，因此我们假设LPS也会修饰下丘脑的脂肪因子表达。具有挑战性的LPS（5 mg / kg; sc）雄性CD-1小鼠的体重显着降低（24 h），实时RT-PCR显示rstn，fiaf和细胞因子信号传导3（socs- 3）下丘脑，垂体，皮质和脂肪组织中的mRNA。下丘脑和垂体中的基因表达迅速增加（3-6小时），但在24小时内恢复正常。相反，除了rstn在脂肪中外，注射后24 h皮质和内脏脂肪中靶基因的表达仍然升高。为了更具体地检查下丘脑对LPS的反应，我们在体外直接研究了其对N-1下丘脑神经元的作用。 LPS（25 microg / mL; 3 h）对rstn mRNA无影响，但显着刺激了fiaf和socs-3表达。尽管各种通行费样受体4（TLR4）拮抗剂（单苯二​​酚，PD098059和SB202190）不能阻止LPS诱导的fiaf和socs-3的增加，但它们确实部分减弱了其刺激作用。我们得出的结论是，LPS治疗会增加中枢和可能是神经元的脂肪因子基因的表达，这可能会影响局部组织的修复和功能，但也可能对炎症引起的下丘脑食欲和能量代谢产生下游影响。

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