儿童急性淋巴细胞白血病核转录因子κB的表达及其意义

为了探讨儿童急性淋巴细胞白血病（ALL）NF-κB P65蛋白的表达及意义,应用SP免疫组织化学法检测32例ALL患儿和40例非血液病的对照儿童NF-κBP65蛋白的表达。结果表明：32例ALL患儿的NF-κB P65蛋白的阳性表达率为87.50%（28/32）,表达定位于ALL细胞的胞核及胞浆中,阳性表达率明显高于对照组12.50%（5/40）,两者比较有显著性差异（χ2=40.28,p〈0.01）。在28例ALL患儿组阳性表达者中,弱阳性表达（＋）占10.71%（3/28）,阳性表达（＋＋）占42.86%（12/28）,强阳性表达（＋＋＋）占46.43%（13/28）。正常对照组均为弱阳性表达（5/5）,两者表达程度经Ridit分析差异有显著意义（p〈0.01）。ALL病程间（初发或复发）、免疫表型间（T系ALL与B系ALL）、各细胞形态学间的表达程度差异均无显著意义（p〉0.05,四格表精确概率法）。结论：NF-κB P65蛋白表达于儿童ALL细胞中,抑制NF-κB信号传导途径可能在儿童ALL治疗中有重大价值,这为临床寻求以NF-κB为靶点的治疗手段提供了科学依据。     

中度低温对急性胰腺炎大鼠核转录因子-κB表达的影响

目的观察急性出血坏死性胰腺炎（AHNP）后不同时间点胰腺和肺组织中核转录因子-κB（NF-κB）的DNA结合活性动态变化，以及胰腺炎后应用中度低温对NF-κB活性的影响。方法第一部分实验采用牛磺胆酸钠逆行注射造成大鼠AHNP模型。大鼠随机分为正常对照组以及AHNP常温2、5和12h组，用电泳迁移率改变法（EMSA）测定各组大鼠胰腺和肺组织中NF-κB的活性。第二部分实验将大鼠随机分为假手术组、AHNP常温组和低温组，诱导AHNP后2h和5h测定各组胰腺和肺组织中NF-κB的活性。结果急性胰腺炎后大鼠胰腺和肺组织NF-κB活性均持续增强，且各时间点胰腺组织NF-κB活性显著强于肺组织（P均〈0．01）。与AHNP常温组相比，低温组AHNP后2h和5h肺组织NF-κB活性均显著降低（P均〈0．01），而胰腺组织NF-κB活性与常温组差异不明显。结论急性胰腺炎伴有胰腺和肺组织NF-κB活性的显著增强。中度低温对急性胰腺炎后肺组织NF-κB的激活有抑制作用。     

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.     

核转录因子-κB在急性肾损伤细胞凋亡中的作用

急性肾损伤是临床常见的危重症,病死率高,缺乏有效的防治措施.研究发现,细胞凋亡在急性肾损伤的发生机制中起着重要作用.核转录因子-κB (NF-κB)是具有多向转录调节作用的核蛋白因子,与细胞凋亡关系密切,参与多种凋亡相关基因的转录调控,具有抑制和促进细胞凋亡的双向作用.本文就NF-κB信号传导在急性肾损伤细胞凋亡中的作用作一综述.     

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.     

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.     

脂多糖对中性粒细胞核转录因子-κB活性的影响

目的：探讨在脂多糖（LPS）刺激下,中性粒细胞核转录因子-κB（NF-κB）活性变化及其抑制因子（IκBα）的影响。方法：离体培养人中性粒细胞,分为来普霉素B（LMB）干预组（A组）、LPS刺激组（B组）和LPM＋LPS组（C组）。各组分别在刺激后0、15、60、120min,用NF-κBp65试剂盒检测细胞核NF-κB活性,用Western-blot检测细胞核、浆中IκBα含量。结果：A组中各时相点NF-κB活性无明显变化;同一时相点细胞核、浆之间,以及不同时相点细胞核之间、细胞浆之间IκBα含量无明显变化。B组LPS刺激后,NF-κB活性较0点时明显增强;细胞核、浆中各时相点IκBα较未刺激时显著降低;细胞核、浆中呈现一致性变化。C组NF-κB活性于60min时点后,较B组同时相点明显受抑制;胞浆中IκBα于60min时较B组明显减少,而核中IκBα于60min后较B组明显增加。结论：NF-κB活性与核中IκBα含量呈负相关;IκBα在中性粒细胞存在核浆穿梭,通过抑制IκBα核浆穿梭,可显著降低NF-κB活性。     

褪黑素抑制大鼠急性肺损伤时核转录因子-κB的表达

目的 探讨褪黑素(MT)对大鼠急性肺损伤(ALI)时肺脏的保护作用及其可能机制.方法 将96只SD大鼠随机分为4组:对照组、脂多糖(LPS)组、地塞米松(DEX)和MT组,每组24只.采用气道内滴注LPS制备ALI大鼠模型;DEX和MT干预采用腹腔注射.分别于给药后3、6和12 h活杀各组大鼠取肺组织标本,检测肺组织中髓过氧化物酶(MPO)和超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量;用免疫组化方法检测核转录因子-κB(NF-κB)在肺组织的表达.结果 LPS组各时间点SOD活性较对照组明显降低(P<0.05或P<0.01),而MPO活性与MDA含量以及NF-κB的表达则显著升高(P<0.05或P<0.01);应用MT及DEX均能显著缓解上述变化(P<0.05或P<0.01);上述各指标以6 h变化最为显著,分别达到峰值或谷底.结论 MT对ALI时肺脏的保护作用可能与MT清除自由基及抑制NF-κB的激活有关.     

核转录因子-κB在子宫内膜异位症中的表达及其意义

目的　检测核转录因子 κB(NF-κB)在子宫内膜异位症 (EM)中的表达 ,探讨其与EM发病机制的关系。方法　采用免疫组化SP法检测NF-κB在内膜组织中的表达情况 ,并用组织学评分对其进行半定量统计 ,比较其表达强度。结果　NF-κB主要定位于腺上皮细胞的胞质中 ,在异位内膜的基质细胞、螺旋小动脉的血管内皮细胞也有少量表达。子宫内膜异位症患者中异位内膜组表达强度显著高于在位组及对照组 (P <0.0 1) ,各组中分泌期与增生期表达强度比较前者高于后者 (P <0.0 5 )。结论　NF-κB在EM患者中的异常表达 ,提示其与EM的发病密切相关     

三氧化二砷诱导白血病细胞凋亡与核因子-κB活化的关系

为了研究三氧化二砷（As2O3）诱导白血病细胞凋亡与核因子-κB（NF-κB）活化以及血管内皮生长因子（VEGF）、基质金属蛋白酶-9（MMP9）表达的关系,应用流式细胞仪Annexin V FITC法检测白血病细胞系K562-n凋亡;采用免疫组织化学方法半定量分析K562-n细胞NF-κB、VEGF、MMP9表达的动态变化.结果显示：As2O3在诱导K562-n细胞凋亡的过程中可活化NF-κB,而VEGF、MMP9的表达也随之增强.地塞米松（DXM）1μmol/L能显著增加As2O3诱导K562-n细胞凋亡的作用和抑制K562-n细胞NF-κB活化,细胞凋亡增加率为43.04%,（P＜0.05）,NF-κB活化抑制率为31.15%（P＜0.05）,VEGF、MMP9变化与NF-κB一致.结论：As2O3诱导K562-n细胞凋亡的过程中可使NF-κB活化,VEGF、MMP9表达亦随之增强;DXM可通过抑制NF-κB活化增强其诱导K562-n细胞凋亡的作用,VEGF、MMP9的表达也随之下降.     

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…     

核因子-κB在结肠炎的表达及地塞米松对其影响

目的 :探讨核因子 κB (NF κB )活化在大鼠实验性结肠炎发病中的作用及地塞米松对其的影响。方法 :用TNBS制作大鼠实验性结肠炎模型。将大鼠随机分为对照组 (C组 )、TNBS损伤组 (T组 )、地塞米松治疗组 (D组 )。应用免疫组化方法观察TNBS灌肠后 1、2、4、6周结肠黏膜NF κBp65及IκBα蛋白表达的动态变化。应用原位杂交方法检测NF κBp 65mRNA的表达。结果 :( 1)免疫组化 :T组大鼠结肠黏膜NF κBp65蛋白表达较C组显著增高 (P <0 0 1) ,IκBα表达较C组显著降低 (P <0 0 1) ;D组大鼠结膜黏膜NF κBp65蛋白表达较T组显著降低 (P<0 0 1) ,但显著高于C组 (P <0 0 1) ,IκBα表达较T组显著增高 (P <0 0 1) ,但显著低于C组 (P <0 0 1)。 ( 2 )原位杂交检测 :T组大鼠结肠黏膜NF κBp65mRNA表达明显高于C组 (P <0 0 1) ;D组大鼠结肠黏膜NF κBp65mR NA表达显著高于C组 (P <0 0 1) ,但显著低于T组 (P <0 ,0 1)。结论 :NF κB活化在大鼠实验性结肠炎发病中可能起重要作用 ,地塞米松可能部分地抑制NF κB的活化 ,从而减轻结肠黏膜炎症改变。