文章摘要
陈 涛,朱 洁,张子焕,王玉海,齐一龙.重型颅脑损伤患者血清Arc水平及其与程序性坏死关系的研究[J].,2018,(13):2499-2503
重型颅脑损伤患者血清Arc水平及其与程序性坏死关系的研究
A Study on the Arc Expression and Its Relationship with Necroptosis in Severe Traumatic Brain Injury Patients
投稿时间:2018-01-24  修订日期:2018-02-21
DOI:10.13241/j.cnki.pmb.2018.13.020
中文关键词: 重型颅脑损伤  Arc蛋白  程序性坏死  炎性细胞因子
英文关键词: Severe traumatic brain injury  Arc protein  Necroptosis  Inflammatory cytokines
基金项目:国家自然科学基金项目(81701932)
作者单位E-mail
陈 涛 解放军第123医院神经外科 安徽 蚌埠 233000安徽医科大学无锡临床学院解放军第101医院神经外科 江苏 无锡 214044 fmmuchentao@163.com 
朱 洁 安徽医科大学无锡临床学院解放军第101医院神经外科 江苏 无锡 214044  
张子焕 解放军第123医院神经外科 安徽 蚌埠 233000  
王玉海 安徽医科大学无锡临床学院解放军第101医院神经外科 江苏 无锡 214044  
齐一龙 解放军第123医院神经外科 安徽 蚌埠 233000  
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中文摘要:
      摘要 目的:探讨重型颅脑损伤(sTBI)患者血清Arc蛋白表达及其与神经元程序性坏死的关系。方法:采用回顾性研究的方法,选取中国人民解放军第123医院神经外科自2013年6月至2017年4月收治的sTBI患者55例(sTBI组)和同期该院体检中心健康体检者55例(Control组),将sTBI组患者分为Arc蛋白低表达组(小于150.37 pg/mL,sTBI-L)和Arc蛋白高表达组(大于150.37 pg/mL,sTBI-H)。采用酶联免疫吸附法(ELISA)检测受试者外周血Arc蛋白含量,采用蛋白质印迹法(Western blot)检测程序性坏死相关蛋白受体相互作用蛋白激酶1(RIPK1)、受体相互作用蛋白激酶3(RIPK3)和混合系激酶区域样蛋白(MLKL)的表达,采用ELISA法检测炎症因子白介素1β(IL-1β)、肿瘤坏死因子α(TNF-α)和白介素10(IL-10)的表达。结果:sTBI组血清Arc蛋白含量明显高于Control组(150.37 ± 21.08 pg/mL vs. 87.65 ± 13.43 pg/mL),差异有统计学意义(P < 0.001)。与Control组比较,sTBI-L组、sTBI-H组RIPK1、RIPK3和MLKL表达均明显增高(P < 0.001);与sTBI-H组比较,sTBI-L组RIPK3和MLKL表达明显增高(P<0.001),而RIPK1表达无差异(P=0.181)。与Control组比较,sTBI-L组、sTBI-H组血清IL-1β、TNF-α和IL-10表达均明显增高(P<0.001);与sTBI-H组比较,sTBI-L组血清IL-1β和TNF-α表达明显增高(P = 0.027,0.008),而IL-10表达明显降低(P = 0.015)。结论:重型颅脑损伤患者血清Arc蛋白表达增加,可能介导了神经元程序性坏死和炎症反应。
英文摘要:
      ABSTRACT Objective: To investigate the expression of Arc protein in serum and its relationship with neuronal necroptosis in severe traumatic brain injury (sTBI) patients. Methods: This is a retrospective study. Fifty-five sTBI patients, admitted to the department of neurosurgery in the 123th Hospital of PLA from June 2013 to April 2017, were selected as the sTBI group (sTBI), and 55 healthy subjects accepted physical examination at the same period in the same hospital were selected as the control group (Control). The patients in sTBI group were further divided into low Arc level group (< 150.37 pg/mL, sTBI-L) and high Arc level group (> 150.37 pg/mL, sTBI-H). The enzyme linked immunosorbent assay (ELISA) was performed to determine the protein levels of Arc in serum. Western blot was performed to detect the expression of necroptosis-associated factors, including receptor protein interacting kinase 1 (RIPK1), receptor protein interacting kinase 3 (RIPK3) and mixed lineage kinase domain-like (MLKL). ELISA was also used to measure the levels of inflammatory cytokines, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10). Results: The protein level of Arc in sTBI group was higher than that in Control group (150.37 ± 21.08 pg/mL VS. 87.65 ± 13.43 pg/mL), and the difference was statistically significant (P < 0.001). The expression of RIPK1, RIPK3 and MLKL in sTBI-L or sTBI-H group was higher than that in Control group (P < 0.001). The expression of RIPK3 and MLKL in sTBI-L group was higher than that in sTBI-H group (P < 0.001), but the expression of RIPK1 in sTBI-L group and sTBI-H group were not statistically different (P = 0.181). The levels of IL-1β, TNF-α and IL-10 in sTBI-L or sTBI-H group was higher than that in Control group (P < 0.001). The levels of IL-1β and TNF-α in sTBI-L group was higher than that in sTBI-H group (P = 0.027 or 0.008), whereas the levels of IL-10 in sTBI-L group were lower than that in sTBI-H group (P = 0.015). Conclusion: The expression of Arc protein is significantly increased in serum of sTBI patients, and its expression is associated with neuronal necroptosis and inflammatory factors.
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