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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Pain regulation of endokinin A/B or endokinin C/D on chimeric peptide MCRT in mice
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Pain regulation of endokinin A/B or endokinin C/D on chimeric peptide MCRT in mice

机译：小鼠嵌合肽MCRT对内皮激肽A / B或内皮激肽C / D的疼痛调节

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摘要

The present study focused on the interactive pain regulation of endokinin A/B (EKA/B, the common C-terminal decapeptide in EKA and EKB) or endokinin C/D (EKC/D, the common C-terminal duodecapeptide in EKC and EKD) on chimeric peptide MCRT (YPFPFRTic-NH2, based on YPFP-NH2 and PFRTic-NH2) at the supraspinal level in mice. Results demonstrated that the co-injection of nanomolar EKA/B and MCRT showed moderate regulation, whereas 30 pmol EKA/B had no effect on MCRT. The combination of EKC/D and MCRT produced enhanced antinociception, which was nearly equal to the sum of the mathematical values of single EKC/D and MCRT. Mechanism studies revealed that pre-injected naloxone attenuated the combination significantly compared with the equivalent analgesic effects of EKC/D alone, suggesting that EKC/D and MCRT might act on two totally independent pathways. Moreover, based on the above results and previous reports, we made two reasonable hypotheses to explain the cocktail-induced analgesia, which may potentially pave the way to explore the respective regulatory mechanisms of EKA/B, EKC/D, and MCRT and to better understand the complicated pain regulation of NK1 and mu opioid receptors, as follows: (1) MCRT and endomorphin-1 possibly activated different mu subtypes; and (2) picomolar EKA/B might motivate the endogenous NPFF system after NK1 activation.
机译：本研究集中于内皮激肽A / B（EKA / B，EKA和EKB中常见的C端十肽）或内皮激肽C / D（EKC / D，EKC和EKD中常见的C端十二肽）的交互性疼痛调节。 ）在小鼠脊髓上层水平的嵌合肽MCRT（YPFPFRTic-NH2，基于YPFP-NH2和PFRTic-NH2）上）。结果表明，纳摩尔EKA / B和MCRT的共同注射显示出中等程度的调节作用，而30 pmol EKA / B对MCRT没有影响。 EKC / D和MCRT的结合产生了增强的抗伤害感受，几乎等于单个EKC / D和MCRT的数学值之和。机制研究表明，与单独的EKC / D的等效镇痛作用相比，预注射的纳洛酮可显着减弱该组合，这表明EKC / D和MCRT可能在两种完全独立的途径上起作用。此外，基于以上结果和先前的报道，我们做出了两个合理的假设来解释鸡尾酒引起的镇痛，这可能为探索EKA / B，EKC / D和MCRT的各自调节机制铺平了道路，了解NK1和mu阿片受体的复杂疼痛调节，如下：（1）MCRT和endomorphin-1可能激活了不同的mu亚型; （2）NK1激活后，皮摩尔EKA / B可能会刺激内源性NPFF系统。

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