创伤性休克伴SIRS患者血浆循环S100A8/S100A9相关通路蛋白的表达研究  

Expression of S100A8/S100A9-related Pathway Proteins in Plasma Circulation in Patients with Traumatic Shock and SIRS

作　　者：关永佳 董君博 王慧萍 范银强 刘玉鹏 李瑞金 易骏 王爽 GUAN Yong-jia;DONG Jun-bo;WANG Hui-ping;FAN Yin-qiang;LIU Yu-peng;LI Rui-jin;YI Jun;WANG Shuang(Emergency Department,Southeastern Central Hospital,Dongguan City,Guangdong,523710)

机构地区：[1]广东省东莞市东南部中心医院急诊科,523710

出　　处：《岭南急诊医学杂志》2024年第5期449-452,共4页Lingnan Journal of Emergency Medicine

基　　金：广东省东莞市社会发展科技项目(20231800937572)。

摘　　要：目的:探讨创伤性休克伴SIRS患者血浆循环S100A8/S100A9相关通路蛋白表达及意义。方法:采用前瞻性研究方法,纳入我院2022年1月-2024年1月诊断为创伤性休克90例,其中伴SIRS患者43例,另征集健康体检者45例为对照组,检测各组血浆循环S100A8/A9和炎性因子的表达。建立创伤性休克伴SIRS的大鼠模型,采用qRT-PCR和Western Blot检测S100A8/A9水平。结果:创伤性休克伴SIRS患者血浆S100A8/A9及IL-6、TNF-β水平均明显高于创伤性休克组和对照组(P<0.05);模型组大鼠血浆S100A8/A9蛋白浓度和IL-6、TNF-β亦显著升高,同时肺、肝组织中S100A8-mRNA、S100A9-mRNA和S100A8/A9蛋白水平也明显高于对照组(P<0.05)。相关分析显示,大鼠循环血浆S100A8/A9水平与炎性因子IL-6、TNF-β均呈正相关(r=0.874,0.748,P=0.000)。结论:S100A8/A9作为新的炎症介质参与了创伤性休克患者SIRS的发生发展,其机制可能与促炎因子TNF-ɑ、IL-6产生协同作用,共同加剧创伤性休克伴SIRS的脏器损伤。Objective:To investigate the expression of S100A8/S100A9 related pathways in patients with traumatic shock and SIRS.Methods:90 patients diagnosed with traumatic shock in our hospital were included in the prospective study,including 43 patients with SIRS,and 45 healthy subjects as the control group.The plasma circulating S100A8/A9 and inflammatory factors in each group were detected.A rat model of traumatic shock with SIRS was established,and S100A8/A9 levels were detected by qRT-PCR and Western Blot.Results:The plasma levels of S100A8/A9 andIL-6 and TNF-βin the patients with traumatic shock and SIRS were significantly higher than those in the patients without SIRS and control group(P<0.05).Plasma S100A8/A9 protein,IL-6 and TNF-βwere also significantly increased in model group,while S100A8-mRNA,S100A9-mRNA and S100A8/A9 protein levels in lung and liver tissues were also significantly higher than those in control group(P<0.05).Correlation analysis showed that the levels of circulating plasma S100A8/A9 were positively correlated with inflammatory cytokines IL-6 and TNF-β(r=0.874,0.748,P=0.000).Conclusion:As a new inflammatory mediator,S100A8/A9 participated in the occurrence and development of SIRS in patients with traumatic shock.Its mechanism may have synergistic effect with pro-inflammatory factor TNf-alpha and IL-6,which jointly exacerbated the organ injury of traumatic shock accompanied by SIRS.

关 键 词：创伤性休克 SIRS 血浆循环S100A8/S100A9 

分 类 号：R605.971[医药卫生—急诊医学]