核因子-κB--急性肺损伤基因治疗的新焦点

核顺子-κB(NF-κB)是一类能与多种基因启动子部位的κB位点发生特异性结合并促进转录的蛋白质的总称.体内外实验发现,NF-κB活化与TNF-α、IL-6、IL-8、ICAM-1、VCAM-1等细胞因子的基因过度表达有关,后者在急性肺损伤(ALI)的发病中起着重要作用.NF-κB的激活可能是ALI的重要发病机制.因此,通过抑制NF-κB的激活能对ALI起到防治作用.     

核因子-κB与急性肺损伤

核因子-κB是一种对许多参与免疫与炎症反应等有关基因的表达具有调控作用的转录因子。其在急性肺损伤发 病机制及诊疗中的作用已日益引起人们关注。本文就核因子-κB构成、活化、生物学效应及其在急性肺损伤中的作用作一综 述。     

核因子-κB与肝移植

核因子-κB（nuclear factor-κB，NF—κB）首先是由Sen和Baltimore于1986年报道，他们从成熟的B细胞核抽提物中发现的一种能与免疫球蛋白κ链基因增强子KB序列5-GGGRNNYYCC-3特异性结合的核蛋白因子．该因子与κ链的结合可促进κ链基因的表达。随后人们发现NF-κB是一种重要的核转录因子，几乎存在于所有细胞，调节超过150种基因的表达，这些基因涉及细胞活动的许多领域，包括炎症反应、免疫应答、细胞增殖分化、细胞凋亡等生理和病理活动。近年，由于器官移植基础研究迅猛发展，NF-κB在器官保存、缺血再灌注损伤、急慢性排斥反应、免疫抑制药物作用机制等方面的作用逐渐引起人们注意。本文就其结构、功能及其在肝移植中的作用进行综述。     

p38MAPK抑制剂对急性肺损伤大鼠肺组织核因子-κB表达的影响

目的 观察p38丝裂原活化蛋白激酶（p38MAPK）抑制剂预处理对大鼠内毒素型急性肺损伤（Au）核因子-κB（NF-κB）的影响。方法 腹腔内注射＋气管内给内毒素复制大鼠ALI模型，用免疫组化方法测定肺组织NF-κB的表达。结果实验组、预处理组NF-κB的表达高于对照组（P〈0．05或P〈0．01），且实验组高于预处理组（P〈0．05）。结论 p38MAPK抑制剂可减轻大鼠细胞的NF-κB表达，减轻肺组织的病理损害。     

核因子—κB与急性肺损伤

核因子-κB是一种对许多参与免疫与炎症反应等有关基因的表达具有调控作用的转录因子。其在急性肺损伤发病机制及诊疗中的作用已日益引起人们关注。本文就核因子-κB构成、活化、生物学效应及其在急性肺损伤中的作用作一综述。     

胃癌组织中核转录因子-κB表达与意义

核转录因子-κB（NF-κB）是一种转录因子、调节许多基因的表达。我们通过免疫组织化学检测了53例胃癌及18例正常胃组织中NF-κB的表达及分析其与胃癌生物学行为的关系。     

核因子-κB活化在大鼠急性坏死性胰腺炎肺损伤中的作用

通过急性坏死性胰腺炎 (ANP)模型 ,探讨核因子 κB(NF κB )活化在大鼠ANP肺损伤发病机制中的作用。一、材料与方法1.实验动物分组与模型 :雄性Wistar大鼠 ,体重 2 0 0～ 2 5 0g ,随机分成 3组 ,对照组、ANP组、NF κB抑制剂二硫代氨基甲酸吡咯烷 (PDTC)组 ,每组 30只。大鼠禁食 2 4h ,自由饮水。 2 5 %戊巴比妥钠腹腔注射麻醉 ,胰管末端逆行穿刺 ,近肝门及十二指肠乳头处夹闭胰管两端 ,1ml/kg体重胰管内缓慢匀速注入 5 %牛磺胆酸钠。对照组胰管内注入等量0 9%生理盐水。模型制备后 ,PDTC组立即尾静脉缓慢匀速注入PDTC 10mg/…     

核因子-κB及其在子宫内膜表达的研究进展

核因子 kappa B(nuclearfactorkappaB ,NF κB)是一类普遍存在的转录因子 ,可与核内基因上启动子区域的固定核苷酸序列结合 ,由此调节多种编码细胞因子、生长因子、细胞粘附分子的基因。本文简要介绍其分子结构及特征 ,并综述人子宫内膜NF κB的表达、NF κB与细胞因子的相互调节和性激素对NF κB的影响等的研究进展。     

核转录因子-κB与肾间质纤维化

核转录因子-κB是一种具有多向性调节作用的核转录因子,参与了许多肾脏疾病发生发展过程。肾间质纤维化是各种慢性肾脏疾病进展到终末期肾衰竭的共同通路,NF-κB通过对小管上皮细胞、间质炎症、各种炎症细胞因子等方面参与肾纤维化过程。本文从上述各方面综述了近年来NF-κB在肾纤维化方面的研究进展。     

核因子-κB介导脂多糖诱导急性肺损伤大鼠高迁移率族蛋白B1的表达

目的探讨核因子(NF)-κB在脂多糖诱导大鼠急性肺损伤过程中对肺组织高迁移率族蛋白B1(HMGB1)表达的影响。方法采用腹腔注射脂多糖(LPS)致大鼠脓毒症急性肺损伤模型。取健康SPF级雄性SD大鼠72只,体重180~220g,采用随机数字表法,分为对照组(C组,n=6)、急性肺损伤组(L组,n=30)、吡咯烷二硫代氨基甲酸盐(PDTC)溶剂对照组(P组,n=6),PDTC治疗组(LP组,n=30)。各组分别给予腹腔注射磷酸盐缓冲液(PBS)(C和P组)或LPS(L和LP组);P组和LP组在PBS或LPS注射前15min,给予腹腔注射PDTC 100mg/kg。C组和P组腹腔注射PBS后的16h,L组和LP组注射LPS后的16h后各取6只大鼠检测其肺湿/干重比(W/D);C组和P组腹腔注射PBS后的16h,L组和LP组注射LPS后的4h(T1)、8h(T2)、16h(T3)、24h(T4)和48h(T5)时各取6只大鼠经处理后采用ELISA法检测支气管肺泡灌洗液(BALF)中髓过氧化物酶(MPO)和白细胞介素6(IL-6)水平,Western blot法检测肺组织HMGB1的表达水平,苏木精-伊红(HE)染色观察肺组织的病理变化。结果与C组比较,L组肺组织W/D、BALF中MPO和IL-6水平明显升高(P0.01),病理切片显示严重肺组织损伤,T2~T4时肺组织中HMGB1的表达水平明显升高(P0.05);使用PDTC治疗后,与L组比较,肺组织W/D、BALF中MPO和IL-6水平明显降低(P0.01),病理示肺损伤程度明显减轻;T2~T4时肺组织HMGB1表达水平明显降低(P0.05)。结论在脂多糖诱导急性肺损伤中,被激活的NF-κB通过介导晚期炎症因子HMGB1的表达来参与急性肺损伤的发生与发展过程。     

糖尿病与核转录因子NF-κB

核转录因子-κB(NF-κB)作为一种转录调节因子在体内各组织细胞中广泛存在，调控多种细胞因子和炎性介质的基因表达，调节免疫反应，与多种疾病的发生发展密切相关。了解其生物学特点，与肾脏病的关系。特别是近年来在糖尿病及糖尿病肾病发病中的作用，有助于该病的防治。     

雾化吸人利多卡因对哮喘大鼠肺组织热休克蛋白70、核因子κB表达的影响

目的 观察利多卡因对大鼠支气管哮喘模型肺组织中热休克蛋白70(heat shock protein 70,HSP70)、核因子κB(nuclear factor-kappe B,NF-κB)表达的影响.方法 Wistar大鼠32只,随机分为4组(n=8):对照组(A组)、哮喘组(B组)、地塞米松组(C组)、利多卡因组(D组).B组大鼠用鸡卵清蛋白辅以氢氧化铝为佐剂注射致敏,2周后雾化吸入鸡卵清蛋白诱发哮喘;C组、D组大鼠用同样方法致敏,但在激发前分别雾化吸入0.02%地寒米松和0.04%利多卡因20 ml;A组用生理盐水代替鸡卵清蛋白进行注射和吸入.末次雾化吸人后24 h内取肺组织,计算湿十重比(W/D)、观察肺组织病理学改变、免疫组化检测HSP70、NF-κB的表达.结果 ①B、C、D组W/D值分别为4.08±0.16、3.54±0.10和3.66±0.12,和A组3.30±0.12相比增加(P<0.05);②B、C、D组肺组织HSP70表达分别为0.210±0.018、0.138±0.010和0.154±0.012,和A组0.049±0.015相比表达上调(P<0.05);③B、C、D组肺组织NF-κB表达分别为0.199±0.029、0.132±0.010和0.150±0.017,和A组0.056±0.022相比表达上调(P<0.05);④和B组相比,C、D组W/D值、肺组织HSP70、NF-κB的表达下调(P<0.05).B组肺组织呈支气管壁增厚、炎性细胞浸润表现.C组、D组病理损伤程度减轻. 结论利多卡因雾化吸入可以减轻致敏原所激发的哮喘大鼠气道炎症和肺组织损伤.     

雾化吸人利多卡因对哮喘大鼠肺组织热休克蛋白70、核因子κB表达的影响

Objective To observe the effect of aerosolized lidocaine inhalation on expression of HSP70 and NF-ΚB in lung of asthma rat model. Methods Thirty two Wistar rats were randomly assigned to four groups (n=8 each): control group( group A), asthma model group(group B),dexamethasone group(group C)and lidocaine group(group D). The rats in group B were sensitized by injection of ovalbumin(OA )together with aluminum hydroxide as adjuvants, followed by aerosolized OA challenge two weeks later. The rats in group C and D were sensitized with OA as group B, but exposed to 0.02% aerosol of dexamethasone and 0.04% aerosol of lidocaine 20 ml respectively. In group A saline was used instead of OA. In 24 hours after the last challenge, the lungs were removed for microscopic examination, determination of W/D lung weight radio, the expression of HSP70 and NF-ΚB was studied immunohistochemically.Results①The W/D lung weight radio were 4.08±0.16,3.54±0.10 and 3.66±0.12 respectively in group B,C,D,more than the group A with 3.30±0.12. ② The pulmonary expression of HSP70 were 0.210±0.018,0.138±0.010 and 0.154±0.012 respectively in group B,C,D, higher than the group A with 0.049±0.015. ③The pulmonary expression of NF -KB were 0.199±0.029,0.132±0.010 and 0.150±0.017respectively in group B, C, D, higher than the group A with 0.056±0.022. ④Compared with the group B, the W/D lung weight radio and pulmonary expression of HSP70 and NF -ΚB in group C and D were significantly down -regulated. In animals with asthma the bronchial walls were significantly thicker with inflammatory cell infiltration. Dexamethasone or lidocaine aerosolized inhalation significantly attenuated the pathologic changes induced by asthma. Conclusion Aerosolized lidocaine inhalation has a protective effect on airway inflammation and histology damages resulting from aeroallergen challenge in the asthma model of Wistar rats.     

热休克因子1及其与热休克蛋白表达的关系研究进展

This article reviews the advances in the research of the structural characteristics and the activating process of heat shock factor 1(HSF-1),the factors that influence the expression of HSF-1,and the r...     

雾化吸人利多卡因对哮喘大鼠肺组织热休克蛋白70、核因子κB表达的影响

Objective To observe the effect of aerosolized lidocaine inhalation on expression of HSP70 and NF-ΚB in lung of asthma rat model. Methods Thirty two Wistar rats were randomly assigned to four groups (n=8 each): control group( group A), asthma model group(group B),dexamethasone group(group C)and lidocaine group(group D). The rats in group B were sensitized by injection of ovalbumin(OA )together with aluminum hydroxide as adjuvants, followed by aerosolized OA challenge two weeks later. The rats in group C and D were sensitized with OA as group B, but exposed to 0.02% aerosol of dexamethasone and 0.04% aerosol of lidocaine 20 ml respectively. In group A saline was used instead of OA. In 24 hours after the last challenge, the lungs were removed for microscopic examination, determination of W/D lung weight radio, the expression of HSP70 and NF-ΚB was studied immunohistochemically.Results①The W/D lung weight radio were 4.08±0.16,3.54±0.10 and 3.66±0.12 respectively in group B,C,D,more than the group A with 3.30±0.12. ② The pulmonary expression of HSP70 were 0.210±0.018,0.138±0.010 and 0.154±0.012 respectively in group B,C,D, higher than the group A with 0.049±0.015. ③The pulmonary expression of NF -KB were 0.199±0.029,0.132±0.010 and 0.150±0.017respectively in group B, C, D, higher than the group A with 0.056±0.022. ④Compared with the group B, the W/D lung weight radio and pulmonary expression of HSP70 and NF -ΚB in group C and D were significantly down -regulated. In animals with asthma the bronchial walls were significantly thicker with inflammatory cell infiltration. Dexamethasone or lidocaine aerosolized inhalation significantly attenuated the pathologic changes induced by asthma. Conclusion Aerosolized lidocaine inhalation has a protective effect on airway inflammation and histology damages resulting from aeroallergen challenge in the asthma model of Wistar rats.