参附注射液对内毒素所致大鼠全身炎症反应综合征的作用

目的:探讨参附注射液对内毒素所致大鼠全身炎症反应综合征(SIRS)的治疗作用及其机制.方法:静脉注射脂多糖(LPS)建立大鼠SIRS模型.健康雄性Wistar大鼠45只,按随机数字表法分为假手术对照组(C组)、LPS致伤组(L组)和参附注射液治疗组(T组).L、T组动物制模后分为1、2、4和6 h 4个亚组.在4个时间点分别取血,采用酶联免疫吸附法(ELISA)检测单个核细胞中核转录因子-κB(NF-κB)活性、血清肿瘤坏死因子-α(TNF-α)及白细胞介素-6(IL-6)水平,观察肺脏和肝脏的病理学变化,并与C组比较.结果:L组单个核细胞中NF-κB活性明显增高,2 h最明显(0.604±0.020),显著高于对照组(0.112±0.017);血清TNF-α浓度明显升高,2 h最明显[(1 644.8±25.9)ng/L],显著高于对照组[(55.9±19.2)ng/L];血清IL-6浓度随时间推移不断升高,显著高于对照组.病理结果显示,L组肺泡出血、水肿、大量炎症细胞浸润;肝脏毛细血管扩张、充血、水肿和炎症细胞浸润.参附注射液可以显著降低NF-κB活性、TNF-α及IL-6水平,减轻肺脏和肝脏病理损伤.结论:参附注射液可通过抑制NF-κB活性对大鼠SIRS起保护作用.     

痰热清注射液对脓毒症大鼠核因子-κB活性及生存率的影响

目的:探讨痰热清注射液对脓毒症(sepsis)大鼠核因子-κB(nuclear factor-κB,NF-κB)活性及生存率的影响。方法:采用盲肠结扎穿孔术(cecum ligation perforation,CLP)制备脓毒症模型。112只Wistar大鼠按随机数字表法分为正常对照组、假手术组、模型组和痰热清治疗组,观察模型组及痰热清治疗组大鼠术后7 d的生存率。用ELISA法检测各组NF-κB活性和IL-6的水平。结果:痰热清治疗组7 d生存率明显高于模型组(P<0.05)。与假手术组比较,模型组大鼠外周血单个核细胞NF-κB活性在CLP后2 h明显升高,6 h达到高峰,各时点与假手术组比较差异有显著性(P<0.01);IL-6水平在CLP后6 h明显升高,12 h达到高峰,除2 h时点外,各时点与假手术组比较差异有显著性(P<0.01);与模型组比较,除2 h时点外,痰热清治疗组NF-κB活性和IL-6水平明显降低(P<0.01)。模型组大鼠外周血单个核细胞NF-κB活性与血浆IL-6水平呈明显正相关(r=0.625,P<0.01)。结论:痰热清注射液可明显抑制脓毒症大鼠NF-κB活性及IL-6水平,提高脓毒症大鼠的生存率。     

核因子κB与全身炎症反应综合征

全身炎症反应综合征(SIRS)是指机体在感染因素作用下导致机体的生理损伤和病理改变,释放体液和细胞因子,引发全身过度炎症反应的一种临床过程[1].它能够引起多器官功能障碍综合征(MODS)、急性呼吸窘迫综合征(ARDS),甚至死亡.在其发生发展过程中,许多炎症细胞释放的细胞因子及炎症介质起着抗感染的作用.但过度的或失控的炎症反应又能引起中性粒细胞介导的组织损伤和器官功能紊乱.SIRS的中性粒细胞性炎症反应是由以下物质在局部生成所致:细胞因子、趋化因子、内皮细胞白细胞粘附分子和酶,如诱导性一氧化氮合成酶(iNOS)和环氧化酶2(COX2).而这些物质的生成受到转录因子复合体核因子κB(nuclear factorkappa B,NFκB)的调节.NFκB作为近年来才发现的具有基因转录调节作用的蛋白质因子,参与了许多炎性因子的调控.因此研究如何抑制NFκB的激活,减少促炎基因的表达,从而减轻组织损伤和炎症反应以改善SIRS患者的预后具有重要意义.     

核因子-κB在大鼠内毒素休克中的作用

目的 探讨核因子-κB(NF-κB)在大鼠内毒素休克中的作用。方法 静脉注射脂多糖(LP)建立大鼠内毒素休克模型。于LPS注射后1、2、4、6h取血，运用ELISA法检测单个核细胞中NF-κB活性、血清中TNF-α及几-6水平，并观测平均动脉压(MAP)、肺脏和肝脏的病理学变化。结果 LPS注射后，血清TNF-α浓度明显升高，2h最明显，显著高于对照组；血清IL-6浓度于LPS注射后，随着时间的推移不断升高，显著高于对照组；MAP随着时间的延长不断下降，各时间点增多显著低于对照组。内毒素休克大鼠的病理结果显示，肺泡出血、水肿、大量炎性细胞浸润；肝脏毛细血管扩张、充血、水肿和炎性细胞浸润。结论 NF-κB可通过上调NTF-α及IL-6的表达，在内毒素休克的发生发展过程中发挥重要作用。     

核因子κB在全身炎症反应综合征和多器官功能障碍综合征中的作用

全身炎症反应综合征 (ＳＩＲＳ)和多器官功能障碍综合征(ＭＯＤＳ)是全身性感染、创伤、烧伤、重症胰腺炎、心肺脑复苏等疾病中存在的一个共同的难点问题。炎症细胞释放的细胞因子及炎性介质在其发病过程中起着保护机体的作用 ,但过度或失控的炎症反应又能引起组织损伤和器官功能紊乱。ＳＩＲＳ/ＭＯＤＳ中致炎因子的过度生成和中性粒细胞、单核 /巨噬细胞的凋亡障碍是导致疾病发生恶化的两个重要因素 ,而这两个方面都与转录因子复合体核因子κＢ(Ｎｕｃｌｅａｒｆａｃｔｏｒ -κＢ ,ＮＦ -κＢ)的参与和调节有关。1　ＮＦ -κＢ的生物学特…     

痰热清注射液治疗小儿肺炎合并全身炎症反应综合征的疗效分析

目的观察分析痰热清注射液佐治小儿肺炎合并全身炎症反应综合征的临床疗效。方法选取该院2010年10月至2012年lO月小儿肺炎合并全身炎症反应综合征的患儿86例,按照数字表随机抽取法分为观察组与对照组,各为43例。对照组采取常规治疗,观察组在常规治疗上给予痰热清注射液辅助治疗,观察比较两组的治疗效果。结果观察组治疗7d总有效率为93．0％（40／43）,对照组治疗7d总有效率为67．4％（29／43）,两组治疗效果对比差异有统计学意义（P〈0．05）。结论痰热清注射液佐治小儿肺炎合并全身炎症反应综合征的临床疗效显著,对比常规治疗优势更为突出。     

大黄素对重症胰腺炎大鼠核转录因子-κB表达变化的影响

目的:观察大黄素对急性坏死性胰腺炎(ANP)大鼠核转录因子-κB(NF-κB)变化的影响,探讨大黄素治疗ANP的作用机制.方法:将60只SD大鼠随机分为假手术组、ANP组、大黄素治疗组;观察各组大鼠血清淀粉酶、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)含量及胰、肺组织NF-κB活化表达.结果:与假手术组比较,ANP组TNF-α、IL-6含量均明显升高,胰、肺组织 NFκB表达亦增加(P均<0.01).应用大黄素治疗后,其各项指标均显著低于ANP组,胰、肺组织NF-κB活化表达降低(P均<0.01),24 h大鼠死亡率低于ANP组(P<0.05).结论:大黄素治疗ANP的作用机制可能是通过抑制NF-κB活化、下调细胞因子表达来减轻ANP的炎症反应.     

内毒素耐受及其与核转录因子-κB的关系

内毒素多次刺激单核/巨噬细胞后可产生内毒素耐受现象,其机制主要为内毒素信号转导功能障碍导致核转录因子-κB(NF-κB)转位受损.创伤、脓毒症、内毒素血症和全身炎症反应综合征(SIRS)患者均具有内毒素耐受特征,内毒素耐受现象应用于临床可能会降低脓毒症和SIRS患者的病死率.     

全身炎症反应综合征患者核因子-κB活性与预后的关系

目的　观察全身炎症反应综合征 (SIRS)患者核因子 κB (NF κB)的活性、白介素 6 (IL 6 )水平及急性生理与慢性健康评分Ⅱ (APACHEⅡ )的变化 ,探讨NF κB活性与SIRS患者病情及预后的关系。方法　将 35名SIRS患者按MODS的诊断标准和疾病的转归分别分成多器官功能障碍综合征组 (MODS组 )和非MODS组 ,存活组和死亡组 ;选择健康体检者 2 0例作为对照组。检测外周血单个核细胞NF κB的活性及血浆IL - 6水平 ,并进行APACHEⅡ评分。结果　SIRS患者的NF κB活性和IL 6水平明显高于对照组 (P<0 0 1) ;NF κB活性 ,IL 6水平和APACHEⅡ评分在MODS组和死亡组分别明显高于非MODS组和存活组(P <0 0 1或P <0 0 5 ) ;NF -κB活性与IL - 6水平及APACHEⅡ评分均呈明显正相关 (r =0 75 4 ,r =0 737,P <0 0 1) ;IL - 6水平与APACHEⅡ评分呈明显正相关 (r=0 6 35 ,P <0 0 1)。结论　NF -κB活性与SIRS患者的病情及预后密切相关     

调控NF—κB／ⅠκB炎症信号转导通路对MODS大鼠炎性反应的影响

目的 建立大鼠MODS模型，将ⅠκB通过腺病毒载体导人体内，以了解其对MODS大鼠炎性反应的影响。方法 50只大鼠随机分为五组：A组（正常对照组），B组（MODS损伤1d组），C组（MODS损伤7d组），D组（腺病毒转载ⅠκB治疗1d组），E组（腺病毒转载ⅠκB治疗7d组）。观察五组大鼠从致伤开始后1、7d的各脏器功能的生化指标，病理组织学及血清TNF—α、IL-6的表达。结果 经中心静脉途径导入腺病毒转载的ⅠκB基因，可降低MODS大鼠血肌酐、谷丙转氨酶、总胆红素、肌酸磷酸肌酶水平，改善动脉血氧分压；减轻大鼠病理组织学损伤，降低血液中TNF—α、IL-6含量。结论 通过中心静脉途径注入腺病毒转载的ⅠκB基因，直接增加了体内ⅠκB的表达，抑制了NF—κB的活化，阻断其所调控的炎症因子的合成，从而消除炎性细胞在体内的大量聚集最终达到阻断炎症反应的恶性循环，成为治疗MODS新的方向。     

核转录因子-κB信号通路在内毒素致急性肺损伤中的作用

急性肺损伤 (acutelunginjury ,ALI)是由各种致病因素(如创伤、休克、感染、中毒等 )导致的急性进行性呼吸衰竭 ,严重的ALI被定义为急性呼吸窘迫综合征 (ARDS)。在细胞水平上它表现为单核 /巨噬细胞、中性粒细胞 (PMN)等炎性细胞的浸润 ;在分子水平上则表现为众多炎症细胞因子、黏附分子的过度表达 ,伴有多种炎症介质的产生。内毒素损害是导致ALI发病的最常见形式之一 ,对其致病机制的研究现已逐渐深入到分子及信号转导水平。内毒素可通过激活多条信号转导通路最终将胞外信号转变为核内信号 ,其中 ,核转录因子 -κB(nuclearfactorofk…     

地塞米松对脑损伤大鼠核转录因子-κB水平的影响

目的 探讨地塞米松对大鼠重度创伤性颅脑损伤(TBI)后脑组织中核转录因子-κB(NF-κB)的影响.方法 将Wistar大鼠随机分为TBI组和地塞米松治疗组,采用气体冲击致大鼠重度TBI模型.各组于术后0、6、24、72、120 h取5只大鼠活杀,取脑组织,苏木素-伊红(HE)染色观察脑组织病理学变化.免疫组化检测脑组织中NF-κB水平.结果 TBI后6 h大鼠脑组织中NF-κB表达即显著升高(P<0.05),于伤后24 h达峰值(P<0.01),之后有所回降.至120 h仍维持较高水平(P<0.05或P<0.01).经地塞米松治疗后6、24、72 h脑组织中NF-kB显著低于TBI组(P均<0.01).结论 大鼠TBI后早期脑组织中NF-κB即反应性升高,并维持较高水平,引起炎症级联反应,导致TBI后继发性损伤.地塞米松可抑制NF-κB,减轻紊乱的炎症细胞因子所致的继发性损伤,起到治疗与保护作用.     

调控NF-κB/IκB炎症信号转导通路对MODS大鼠炎性反应的影响

目的建立大鼠MODS模型,将IκB通过腺病毒载体导入体内,以了解其对MODS大鼠炎性反应的影响。方法50只大鼠随机分为五组:A组(正常对照组),B组(MODS损伤1d组),C组(MODS损伤7d组),D组(腺病毒转载IκB治疗1d组),E组(腺病毒转载IκB治疗7d组)。观察五组大鼠从致伤开始后1、7d的各脏器功能的生化指标,病理组织学及血清TNF-α、IL-6的表达。结果经中心静脉途径导入腺病毒转载的IκB基因,可降低MODS大鼠血肌酐、谷丙转氨酶、总胆红素、肌酸磷酸肌酶水平,改善动脉血氧分压;减轻大鼠病理组织学损伤,降低血液中TNF-α、IL-6含量。结论通过中心静脉途径注入腺病毒转载的IκB基因,直接增加了体内IκB的表达,抑制了NF-κB的活化,阻断其所调控的炎症因子的合成,从而消除炎性细胞在体内的大量聚集最终达到阻断炎症反应的恶性循环,成为治疗MODS新的方向。     

核因子-κB在SIRS的研究进展

全身炎症反应综合征 (ｓｙｓｔｅｍｉｃｉｎｆｌａｍｍａｔｏｒｙｒｅｓｐｏｎｓｅｓｙｎｄｒｏｍｅ,ＳＩＲＳ)是继发于各种打击后全身持续高代谢、高动力循环状态及过度炎症反应 ,是全身炎症反应失控的结果 ,造成多种细胞因子及炎性介质的失控性释放 ,引起正常组织器官的损伤     

地塞米松对脑损伤大鼠核转录因子-κB水平的影响

Objective To explore the effects of dexamethasone on nuclear factor-kB (NF-κB) expression in brain tissue after traumatic brain injury (TBI). Methods Forty rats were randomly divided into two groups: dexamethasone treatment and no treatment, and severe brain injury was produced by gas percussion in both groups. At 0, 6, 24, 72 and 120 hours after injury, 5 rats of each group were executed and the histopathological changes in brain tissue in rats were observed by hematoxylin-eosin (HE) stain. The expression of NF-κB in brain tissue of rats was detected by immunohistochemical method. Results NF-κB expression was significantly up-regulated at 6 hours in brain tissue of rats after TBI (P<0.05), reaching the highest level at 24 hours (P<0. 01). It showed a tendency to lower, but was still high at 120 hours after TBI (P<0. 05 or P<0. 01). After treatment with dexamethasone, NF-κB level was lowered at 6, 24 and 72 hours (all P<0. 01). Conclusion NF-κB expression is up-regulated in brain tissue in early period after TBI, and keeps on a high level, thus inducing inflammatory response to produce secondary injury to brain tissue. Dexamethasone shows protective effects by regulating the levels of NF-κB and prevents secondary injury which is caused by the inflammatory cytokines in rat brain tissue after TBI.     

地塞米松对脑损伤大鼠核转录因子-κB水平的影响

Objective To explore the effects of dexamethasone on nuclear factor-kB (NF-κB) expression in brain tissue after traumatic brain injury (TBI). Methods Forty rats were randomly divided into two groups: dexamethasone treatment and no treatment, and severe brain injury was produced by gas percussion in both groups. At 0, 6, 24, 72 and 120 hours after injury, 5 rats of each group were executed and the histopathological changes in brain tissue in rats were observed by hematoxylin-eosin (HE) stain. The expression of NF-κB in brain tissue of rats was detected by immunohistochemical method. Results NF-κB expression was significantly up-regulated at 6 hours in brain tissue of rats after TBI (P<0.05), reaching the highest level at 24 hours (P<0. 01). It showed a tendency to lower, but was still high at 120 hours after TBI (P<0. 05 or P<0. 01). After treatment with dexamethasone, NF-κB level was lowered at 6, 24 and 72 hours (all P<0. 01). Conclusion NF-κB expression is up-regulated in brain tissue in early period after TBI, and keeps on a high level, thus inducing inflammatory response to produce secondary injury to brain tissue. Dexamethasone shows protective effects by regulating the levels of NF-κB and prevents secondary injury which is caused by the inflammatory cytokines in rat brain tissue after TBI.     

地塞米松对脑损伤大鼠核转录因子-κB水平的影响

Objective To explore the effects of dexamethasone on nuclear factor-kB (NF-κB) expression in brain tissue after traumatic brain injury (TBI). Methods Forty rats were randomly divided into two groups: dexamethasone treatment and no treatment, and severe brain injury was produced by gas percussion in both groups. At 0, 6, 24, 72 and 120 hours after injury, 5 rats of each group were executed and the histopathological changes in brain tissue in rats were observed by hematoxylin-eosin (HE) stain. The expression of NF-κB in brain tissue of rats was detected by immunohistochemical method. Results NF-κB expression was significantly up-regulated at 6 hours in brain tissue of rats after TBI (P<0.05), reaching the highest level at 24 hours (P<0. 01). It showed a tendency to lower, but was still high at 120 hours after TBI (P<0. 05 or P<0. 01). After treatment with dexamethasone, NF-κB level was lowered at 6, 24 and 72 hours (all P<0. 01). Conclusion NF-κB expression is up-regulated in brain tissue in early period after TBI, and keeps on a high level, thus inducing inflammatory response to produce secondary injury to brain tissue. Dexamethasone shows protective effects by regulating the levels of NF-κB and prevents secondary injury which is caused by the inflammatory cytokines in rat brain tissue after TBI.     

地塞米松对脑损伤大鼠核转录因子-κB水平的影响

Objective To explore the effects of dexamethasone on nuclear factor-kB (NF-κB) expression in brain tissue after traumatic brain injury (TBI). Methods Forty rats were randomly divided into two groups: dexamethasone treatment and no treatment, and severe brain injury was produced by gas percussion in both groups. At 0, 6, 24, 72 and 120 hours after injury, 5 rats of each group were executed and the histopathological changes in brain tissue in rats were observed by hematoxylin-eosin (HE) stain. The expression of NF-κB in brain tissue of rats was detected by immunohistochemical method. Results NF-κB expression was significantly up-regulated at 6 hours in brain tissue of rats after TBI (P<0.05), reaching the highest level at 24 hours (P<0. 01). It showed a tendency to lower, but was still high at 120 hours after TBI (P<0. 05 or P<0. 01). After treatment with dexamethasone, NF-κB level was lowered at 6, 24 and 72 hours (all P<0. 01). Conclusion NF-κB expression is up-regulated in brain tissue in early period after TBI, and keeps on a high level, thus inducing inflammatory response to produce secondary injury to brain tissue. Dexamethasone shows protective effects by regulating the levels of NF-κB and prevents secondary injury which is caused by the inflammatory cytokines in rat brain tissue after TBI.     

地塞米松对脑损伤大鼠核转录因子-κB水平的影响

Objective To explore the effects of dexamethasone on nuclear factor-kB (NF-κB) expression in brain tissue after traumatic brain injury (TBI). Methods Forty rats were randomly divided into two groups: dexamethasone treatment and no treatment, and severe brain injury was produced by gas percussion in both groups. At 0, 6, 24, 72 and 120 hours after injury, 5 rats of each group were executed and the histopathological changes in brain tissue in rats were observed by hematoxylin-eosin (HE) stain. The expression of NF-κB in brain tissue of rats was detected by immunohistochemical method. Results NF-κB expression was significantly up-regulated at 6 hours in brain tissue of rats after TBI (P<0.05), reaching the highest level at 24 hours (P<0. 01). It showed a tendency to lower, but was still high at 120 hours after TBI (P<0. 05 or P<0. 01). After treatment with dexamethasone, NF-κB level was lowered at 6, 24 and 72 hours (all P<0. 01). Conclusion NF-κB expression is up-regulated in brain tissue in early period after TBI, and keeps on a high level, thus inducing inflammatory response to produce secondary injury to brain tissue. Dexamethasone shows protective effects by regulating the levels of NF-κB and prevents secondary injury which is caused by the inflammatory cytokines in rat brain tissue after TBI.     

地塞米松对脑损伤大鼠核转录因子-κB水平的影响

Objective To explore the effects of dexamethasone on nuclear factor-kB (NF-κB) expression in brain tissue after traumatic brain injury (TBI). Methods Forty rats were randomly divided into two groups: dexamethasone treatment and no treatment, and severe brain injury was produced by gas percussion in both groups. At 0, 6, 24, 72 and 120 hours after injury, 5 rats of each group were executed and the histopathological changes in brain tissue in rats were observed by hematoxylin-eosin (HE) stain. The expression of NF-κB in brain tissue of rats was detected by immunohistochemical method. Results NF-κB expression was significantly up-regulated at 6 hours in brain tissue of rats after TBI (P<0.05), reaching the highest level at 24 hours (P<0. 01). It showed a tendency to lower, but was still high at 120 hours after TBI (P<0. 05 or P<0. 01). After treatment with dexamethasone, NF-κB level was lowered at 6, 24 and 72 hours (all P<0. 01). Conclusion NF-κB expression is up-regulated in brain tissue in early period after TBI, and keeps on a high level, thus inducing inflammatory response to produce secondary injury to brain tissue. Dexamethasone shows protective effects by regulating the levels of NF-κB and prevents secondary injury which is caused by the inflammatory cytokines in rat brain tissue after TBI.