瑞芬太尼调节MIP-1α/CCR1信号通路对脑梗死大鼠神经炎症的影响  

Impacts of remifentanil on neuroinflammation in rats with cerebral infarction by regulating MIP-1α/CCR1 signaling pathway

作　　者：肖锦亮 汪威廉 但家朋[1] XIAO Jinliang;WANG Weilian;DAN Jiapeng(Department of Anesthesiology,Jingzhou Central Hospital,Jingzhou Hospital Affiliated to Yangtze University,Jingzhou 434000,China)

机构地区：[1]荆州市中心医院,长江大学附属荆州医院麻醉科,荆州434000

出　　处：《中国免疫学杂志》2025年第4期893-897,共5页Chinese Journal of Immunology

基　　金：荆州市2020年医疗卫生科技计划项目(2020HC05)。

摘　　要：目的:探究瑞芬太尼调节CC型趋化因子巨噬细胞炎症蛋白-1α(MIP-1α)/CC型趋化因子受体1(CCR1)信号通路对脑梗死大鼠神经炎症的影响。方法:大鼠随机分为假手术组、模型组、瑞芬太尼组、MIP-1αAb组(MIP-1α中和抗体,10μg)、HY-U00350组(CCR1拮抗剂,100μg),改良Longa线栓法制备大鼠脑梗死模型。神经功能评分法评估大鼠神经功能;ELISA检测血清TNF-α、IL-6和IL-1β水平;HE染色观察大鼠海马组织病理变化,TTC染色检测大鼠脑梗死面积,TUNEL染色检测大鼠脑细胞凋亡率;RT-qPCR检测MIP-1αmRNA、CCR1 mRNA表达;Western blot检测大鼠脑组织MIP-1α、CCR1蛋白表达。结果:与假手术组相比,模型组大鼠海马神经元结构严重损伤,神经功能评分、TNF-α、IL-6和IL-1β水平、凋亡率、脑梗死面积百分比、MIP-1α、CCR1基因和蛋白表达均显著升高(P<0.05);与模型组相比,瑞芬太尼组、MIP-1αAb组、HY-U00350组神经元形态损害显著减轻,神经功能评分、TNF-α、IL-6和IL-1β水平、凋亡率、脑梗死面积百分比、MIP-1α、CCR1基因和蛋白表达均显著降低(P<0.05);MIP-1αAb组与瑞芬太尼组大鼠各检测指标差异均无统计学意义(P>0.05),HY-U00350组MIP-1α基因和蛋白水平显著升高,其余指标差异也均无统计学意义(P>0.05)。结论:瑞芬太尼可降低脑梗死大鼠神经炎症,可能与抑制MIP-1α/CCR1信号通路有关。Objective:To explore impacts of remifentanil on neuroinflammation in rats with cerebral infarction by regulating CC chemokine macrophage inflammatory protein-1α(MIP-1α)/CC chemokine receptor 1(CCR1)signaling pathway.Methods:Rats were randomly grouped into sham group,model group,remifentanil group,MIP-1αAb group(MIP-1αneutralizing antibody,10μg)and HY-U00350 group(CCR1 antagonist,100μg),improved Longa suture method was applied to prepare a rat cerebral infarction model.Neural function scoring method was applied to evaluate neural function of rats;ELISA was applied to detect serum levels of TNF-α,IL-6 and IL-1β;HE staining was applied to observe pathological changes in rat hippocampal tissue,TTC staining method was applied to detect area of cerebral infarction in rats,TUNEL staining was applied to detect apoptosis rate of rat brain cells;RT-qPCR was applied to detect expressions of MIP-1αmRNA and CCR1 mRNA;Western blot was applied to detect expressions of MIP-1αand CCR1 proteins in rat brain tissue.Results:Compared with sham group,hippocampal neuron structure was seriously damaged in model group,neurological function score,levels of TNF-α,IL-6 and IL-1β,apoptosis rate,percentage of cerebral infarction area,expressions of MIP-1α,CCR1 gene and protein were obviously increased(P<0.05);compared with model group,morphological damage of neurons in remifentanil group,MIP-1αAb group and HY-U00350 group was obviously reduced,neurological function score,levels of TNF-α,IL-6 and IL-1β,apoptosis rate,percentage of cerebral infarction area,expressions of MIP-1α,CCR1 gene and protein were obviously reduced(P<0.05);compared with remifentanil group,indicators of rats in MIP-1αAb group had no statistical significance(P>0.05),levels of MIP-1αgene and protein obviously increased in HY-U00350 group,other indicators were also not statistically obvious(P>0.05).Conclusion:Remifentanil can reduce neuroinflammation in rats with cerebral infarction,which may be related to inhibition of MIP-1α/CCR1 signaling pathway.

关 键 词：瑞芬太尼 MIP-1α/CCR1信号通路 脑梗死 神经炎症 

分 类 号：R392[医药卫生—免疫学] R285.5[医药卫生—基础医学]