降钙素基因相关肽
降钙素
降钙素原
肿瘤坏死因子α
内科学
败血症
感染性休克
内分泌学
受体
降钙素受体
细胞因子
受体拮抗剂
敌手
发病机制
医学
化学
神经肽
作者
Guillaume Monneret,Alexandre Pachot,Beatrice Laroche,Josiane Picollet,Jacques Bienvenu
出处
期刊:Cytokine
[Elsevier]
日期:2000-06-01
卷期号:12 (6): 762-764
被引量:62
标识
DOI:10.1006/cyto.1999.0607
摘要
The pathogenesis of septic shock is mainly due to unregulated tumour necrosis factor-alpha (TNF-alpha) production. Procalcitonin (PCT) and calcitonin gene-related peptide (CGRP) are alternative transcription products of the calcitonin gene. Since high PCT levels have been described in human sepsis, and since CGRP inhibits TNF synthesis in rats, we examined the role of these peptides in the regulation of the inflammatory response during septic shock. LPS-induced TNF production was assessed using a human whole blood model. In this model, PCT (10(-7) M) and CGRP (10(-6) M) significantly inhibit TNF production by 27 and 24 % respectively. The effect of CGRP was reversed by CGRP 8-37 (10 microM), an antagonist of CGRP receptor. No effect on interleukin (IL)-1, IL-6 and IL-8 was found. This is the first description of an anti-inflammatory role for PCT and CGRP in humans.
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