异丙酚促进大鼠脑缺血/再灌注中CGRP释放的机制研究

【目的】探讨异丙酚在大鼠脑缺血/再灌注(IR)损伤中是否促进内源性保护物质降钙素基因相关肽(CGRP)的释放及其调节机制。【方法】实验大鼠分为对照组、假手术组、脑IR组及脑IR 异丙酚治疗组,测定CO、放射免疫测定大鼠脑组织中CGRP、cGMP含量,免疫组化测定HO-1的表达。【结果】脑IR期间,脑IR 异丙酚治疗组的HO-1、CO、cGMP和CGRP显著高于脑IR组和假手术组(P<0.05),且HO-1与CO、CO与cGMP、cGMP与CGRP的表达变化呈正相关(P<0.05),假手术组和对照组间相比较差异无显著性。【结论】异丙酚能促进IR期间CGRP的升高,对大鼠脑IR损伤具有明显的保护作用,作用机制之一可能是通过HO-1-CO-cGMP途径促进CGRP的合成和释放,减轻缺血再灌注的损伤反应。

Study on Release of Calcitonin Gene-related Peptide Promoted by Propofol in Rat Cerebral Ischemia/reperfusion and Its Mechanism

[Objective] To study the mechanism of releasing of calcitonin gene-related peptide (CGRP) during cerebral ischemia-reperfusion injury and the effect of propofol (PPF) on it. [Methods] The rats were randomly divided into four groups (n= 20, in each), control group, sham operated group, CIRI group and CIRI PPF group. The contents of HO-1 (heme oxygenase-1), CO (carbon monoxide), cGMP and CGRP in brain tissue were detected by immunohistochemistry and radioimmunoassay, respectively. [Results] Compared with sham operated group, HO-1, CO, cGMP and CGRP significantly increased after cerebral ischemia-reperfusion injury, and there was positive correlation between the increasing of HO-1 and CO, CO and cGMP, cGMP and CGRP (P<0.05). There was no significant difference between control group and sham operated group. [Conclusion] The results indicate that propofol can protect brain from cerebral ischemia-reperfusion injury through promoting CGRP releasing, and HO-1-CO-cGMP pathway may be the mechanism.