一氧化碳中毒后迟发性脑病患者S100β、JNK通路蛋白及相关细胞因子水平变化及其临床意义
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摘要
目的探讨急性一氧化碳中毒后迟发性脑病(delayed encephalopathy after acute carbon monoxide poisoning,DEACMP)患者脑脊液中S100β、Jun氨基末端激酶(jun amino-terminal kinase,JNK)通路蛋白、白细胞介素-4(interleukin-4,IL-4)、IL-10、转化生长因子β1(transforming growth factorβ1,TGF-β1)及干扰素γ(interferon-γ,IFN-γ)的变化及其临床意义。方法选取2010-01—2016-12作者医院收治的DEACMP患者20例(DEACMP组),另收集同期发生一氧化碳中毒但未发生迟发性脑病的患者37例作为对照组,检测两组患者入院后第2天脑脊液中S100β、JNK通路蛋白(JNK1、JNK2)及TNF-ɑ、IL-4、IL-10、TGF-β1、IFN-γ水平,并于治疗2周后对两组患者进行简易精神状态量表(mini-mental state examination,MMSE)评分,分析脑脊液S100β蛋白、JNK通路蛋白及相关细胞因子与MMSE评分的相关性。结果DEACMP组脑脊液中S100β、JNK1、JNK2、TNF-ɑ、IFN-γ水平均高于对照组(P<0.05),而IL-4、IL-10、TGF-β1水平及MMSE评分均低于对照组(P<0.05)。DEACMP组患者MMSE评分与患者脑脊液中S100β、JNK1、JNK2、TNF-ɑ、IFN-γ水平呈负相关(P<0.05),与IL-4、IL-10、TGF-β1水平呈正相关(P<0.05)。结论 DEACMP患者脑脊液中S100β、JNK通路蛋白及相关细胞因子发生明显改变,且其水平与患者恢复期认知功能损害有关。
Objective To explore the changes and its clinical significance of cerebrospinal fluid S100 beta,JNK pathway proteins and interleukin-4(IL-4),IL-10,transforming growth factor beta 1(TGF-beta1)and interferon gamma(IFN-γ)in delayed encephalopathy after acute carbon monoxide intoxication(DEACMP)patients.Methods Twenty patients with DEACMP who were admitted to our hospital from January2010 to December 2016 were enrolled in this study.Thirty-seven patients who had carbon monoxide poisoning but without delayed encephalopathy were selected as the control group during the same period.The levels of S100β,JNK pathway proteins(JNK1,JNK2)and TNF-ɑ,IL-4,IL-10,TGF-β1 and IFN-γin cerebrospinal fluid were measured.After two weeks of treatment,the MMSE scores of the two groups were tested,and the correlations between MMSE score and S100 B protein,JNK pathway proteins,related cytokines were analyzed.Results Compared with the control group,the levels of S100β,JNK1,JNK2,TNF-ɑand IFN-γin the DEACMP group significantly increased(P<0.05),while the levels of IL-4,IL-10 and TGF-β1 significantly decreased(P<0.05).The MMSE score in the DEACMP group was negatively correlated with the levels of S100β,JNK1,JNK2,TNF-ɑand IFN-γ,and positively correlated with the levels of IL-4,IL-10 and TGF-β1(P<0.05).Conclusions The S100 beta,JNK pathway protein and related cytokines in the cerebrospinal fluid of DEACMP patients are significantly altered and related to the cognitive impairment in the patientsrecovery period.
Objective To explore the changes and its clinical significance of cerebrospinal fluid S100 beta,JNK pathway proteins and interleukin-4(IL-4),IL-10,transforming growth factor beta 1(TGF-beta1)and interferon gamma(IFN-γ)in delayed encephalopathy after acute carbon monoxide intoxication(DEACMP)patients.Methods Twenty patients with DEACMP who were admitted to our hospital from January2010 to December 2016 were enrolled in this study.Thirty-seven patients who had carbon monoxide poisoning but without delayed encephalopathy were selected as the control group during the same period.The levels of S100β,JNK pathway proteins(JNK1,JNK2)and TNF-ɑ,IL-4,IL-10,TGF-β1 and IFN-γin cerebrospinal fluid were measured.After two weeks of treatment,the MMSE scores of the two groups were tested,and the correlations between MMSE score and S100 B protein,JNK pathway proteins,related cytokines were analyzed.Results Compared with the control group,the levels of S100β,JNK1,JNK2,TNF-ɑand IFN-γin the DEACMP group significantly increased(P<0.05),while the levels of IL-4,IL-10 and TGF-β1 significantly decreased(P<0.05).The MMSE score in the DEACMP group was negatively correlated with the levels of S100β,JNK1,JNK2,TNF-ɑand IFN-γ,and positively correlated with the levels of IL-4,IL-10 and TGF-β1(P<0.05).Conclusions The S100 beta,JNK pathway protein and related cytokines in the cerebrospinal fluid of DEACMP patients are significantly altered and related to the cognitive impairment in the patientsrecovery period.
引文
[1]余小骊,刘莉琼,吴豫,等.一氧化碳中毒后迟发性脑病与神经免疫的相关性研究[J].临床神经病学杂志,2015,28(3):185-187.
[2]唐庆,李颖,王永义,等.糖皮质激素联合高压氧防治急性一氧化碳中毒迟发性脑病疗效与安全性Meta分析[J].第三军医大学学报,2016,38(2):207-214.
[3]张露勇,张淼,刘师卜,等.神经酰胺通过JNK/c-Jun信号通路诱导胶质瘤细胞自噬性死亡[J].中国康复理论与实践,2015,21(8):905-912.
[4]Silva FP,Schmidt AP,Valentin LS,et al.S100Bprotein and neuron-specific enolase as predictors of cognitive dysfunction after coronary artery bypass graft surgery.[J].Eur J Anaesthesiol,2016,33(9):1.
[5]宋健楠,孙义,张析哲,等.大鼠脑缺血/再灌注后血清S100β蛋白对脑损伤的诊断价值[J].实用医技杂志,2016,23(3):238-240.
[6]王晶,殷亮,吕涌涛,等.S100B在癫痫患者脑脊液和血清中的表达[J].实用医学杂志,2016,32(20):3422-3424.
[7]Yardan T,Cevik Y,Donderici O,et al.Elevated serum S100B protein and neuron-specific enolase levels in carbon monoxide poisoning[J].Am J Emerg Med,2009,27(7):838-842.
[8]Akelma AZ,Celik A,Ozdemir O,et al.Neuron-specific enolase and S100B protein in children with carbon monoxide poisoning:children are not just small adults[J].Am J Emerg Med,2013,31(10):1531.
[9]Brvar M,Mozina H,Osredkar J,et al.S100Bprotein in carbon monoxide poisoning:apilot study[J].Resuscitation,2004,61(3):357-360.
[10]Liu H,Zhang Y,Ren YB,et al.Serum S100Blevel may be correlated with carbon monoxide poisoning[J].Int Immunopharmacol,2015,27(1):69-75.
[11]Phelps-Polirer K,Abt MA,Smith D,et al.Co-Targeting of JNK and HUNK in resistant HER2-positive breast cancer[J].PLos One,2016,11(4):e0153025.
[12]朱雯,王雪蕊,杨静雯,等.针刺对血管性痴呆模型大鼠大脑皮质神经元凋亡及p-JNK表达的影响[J].中医杂志,2017,58(11):956-959.
[13]刘苏,孙李颖,吴勤峰,等.趋化因子CCL2在重度颅脑损伤患者中的表达[J].重庆医学,2016,45(24):3406-3408.
[14]周志天,陆明岳.一氧化碳中毒后迟发性脑病患者血清中白细胞介素4、白细胞介素10、干扰素γ、转换生长因子β1的水平变化及意义[J].中国基层医药,2015,22(13):2028-2030.
[15]林泽辉,李彦军,杜永明,等.急性一氧化碳中毒迟发型脑病IL-10、MDA及IFN-γ水平变化的意义[J].中西医结合心脑血管病杂志,2016,14(17):2063-2065.
[2]唐庆,李颖,王永义,等.糖皮质激素联合高压氧防治急性一氧化碳中毒迟发性脑病疗效与安全性Meta分析[J].第三军医大学学报,2016,38(2):207-214.
[3]张露勇,张淼,刘师卜,等.神经酰胺通过JNK/c-Jun信号通路诱导胶质瘤细胞自噬性死亡[J].中国康复理论与实践,2015,21(8):905-912.
[4]Silva FP,Schmidt AP,Valentin LS,et al.S100Bprotein and neuron-specific enolase as predictors of cognitive dysfunction after coronary artery bypass graft surgery.[J].Eur J Anaesthesiol,2016,33(9):1.
[5]宋健楠,孙义,张析哲,等.大鼠脑缺血/再灌注后血清S100β蛋白对脑损伤的诊断价值[J].实用医技杂志,2016,23(3):238-240.
[6]王晶,殷亮,吕涌涛,等.S100B在癫痫患者脑脊液和血清中的表达[J].实用医学杂志,2016,32(20):3422-3424.
[7]Yardan T,Cevik Y,Donderici O,et al.Elevated serum S100B protein and neuron-specific enolase levels in carbon monoxide poisoning[J].Am J Emerg Med,2009,27(7):838-842.
[8]Akelma AZ,Celik A,Ozdemir O,et al.Neuron-specific enolase and S100B protein in children with carbon monoxide poisoning:children are not just small adults[J].Am J Emerg Med,2013,31(10):1531.
[9]Brvar M,Mozina H,Osredkar J,et al.S100Bprotein in carbon monoxide poisoning:apilot study[J].Resuscitation,2004,61(3):357-360.
[10]Liu H,Zhang Y,Ren YB,et al.Serum S100Blevel may be correlated with carbon monoxide poisoning[J].Int Immunopharmacol,2015,27(1):69-75.
[11]Phelps-Polirer K,Abt MA,Smith D,et al.Co-Targeting of JNK and HUNK in resistant HER2-positive breast cancer[J].PLos One,2016,11(4):e0153025.
[12]朱雯,王雪蕊,杨静雯,等.针刺对血管性痴呆模型大鼠大脑皮质神经元凋亡及p-JNK表达的影响[J].中医杂志,2017,58(11):956-959.
[13]刘苏,孙李颖,吴勤峰,等.趋化因子CCL2在重度颅脑损伤患者中的表达[J].重庆医学,2016,45(24):3406-3408.
[14]周志天,陆明岳.一氧化碳中毒后迟发性脑病患者血清中白细胞介素4、白细胞介素10、干扰素γ、转换生长因子β1的水平变化及意义[J].中国基层医药,2015,22(13):2028-2030.
[15]林泽辉,李彦军,杜永明,等.急性一氧化碳中毒迟发型脑病IL-10、MDA及IFN-γ水平变化的意义[J].中西医结合心脑血管病杂志,2016,14(17):2063-2065.