Key Laboratory of Preclinical Study for New Drugs of Gansu Province, School of Basic Medical Sciences, and Institute of Biochemistry and Molecular Biology, School of Life Science, Lanzhou University, 222 Tian Shui South Road, Lanzhou 730000, PR China.
Peptides. 2011 Apr;32(4):702-6. doi: 10.1016/j.peptides.2010.12.001. Epub 2010 Dec 16.
The endogenous opioid system has been found to be involved in the fever caused by lipopolysaccharide (LPS). Neuropeptide FF (NPFF, FLFQPQRF-NH(2)) is an endogenous peptide known to modulate opioid activity, mainly in the central nervous system. Therefore, those data suggested a link between LPS-induced fever and NPFF systems. Using a model of acute neuroinflammation, we sought to determine the effects of NPFF systems on the fever induced by i.c.v. injection of LPS. Coinjected with different doses of NPFF (10 and 30 nmol), the fever of LPS (125 ng) was not modified. Interestingly, the selective NPFF receptors antagonist RF9 (30 nmol) injected into the third ventricle failed to induce significant effect, but it decreased the fever of LPS (125 ng) after cerebral administration in mice. These results suggest that NPFF receptors activation is required for LPS to produce fever. This interaction is the first evidence that NPFF systems participate in the control of acute neuroinflammation in conscious animals.
内源性阿片系统被发现参与脂多糖 (LPS) 引起的发热。神经肽 FF (NPFF，FLFQPQRF-NH(2)) 是一种内源性肽，已知可调节阿片类活性，主要在中枢神经系统中。因此，这些数据表明 LPS 诱导的发热与 NPFF 系统之间存在联系。使用急性神经炎症模型，我们试图确定 NPFF 系统对侧脑室注射 LPS 引起的发热的影响。与不同剂量的 NPFF（10 和 30 nmol）共注射时，LPS（125 ng）的发热没有改变。有趣的是，选择性 NPFF 受体拮抗剂 RF9（30 nmol）注入第三脑室没有引起显著效果，但它降低了小鼠脑内给予 LPS（125 ng）后的发热。这些结果表明，NPFF 受体的激活是 LPS 产生发热所必需的。这种相互作用首次证明 NPFF 系统参与了清醒动物急性神经炎症的控制。
