Propentofylline 对中性粒细胞的调节作用

本研究探讨Propentofylline对中性粒细胞的调节作用及其它的作用机制。采用鲁米诺依赖的全血化学发光法测定fMLP激活的中性粒细胞产生过氧化氢。结果显示Propentofylline以浓度依赖形式抑制中性粒细胞产生过氧化氢,并增强腺苷对中性粒细胞的抑制作用,但不影响NECA对中性粒细胞的抑制作用。结果提示,Propentofylline通过抑制细胞对腺苷的提取,增加局部腺苷水平,增强腺苷对中性粒细胞的抑制作用。这种作用也可能是Propentofylline保护心脑组织损伤的机制之一。     

中性粒细胞凋亡分子机制的研究进展

中性粒细胞凋亡在炎性疾病演变过程中起重要作用。多种外界因素可调控中性粒细胞凋亡。其分子机制目前尚不完全明了：最近研究表明抗凋亡蛋白Mcl-1,A1是调控中性粒细胞凋亡的主要因素，MAPK，NF－κB介导了共信号转导过程；凋亡中性粒细胞的内在生化改变和细胞表面分子标志物改变，是吞噬细胞识别，清除的基础。     

人中性粒细胞弹性蛋白酶抑制剂的研究进展

人中性粒细胞弹性蛋白酶(human neutrophil elastase, hNE)是一种丝氨酸蛋白水解酶,主要分布于中性粒细胞中。当体内抗hNE蛋白与hNE的平衡被打破,过量释放的hNE会导致相关疾病的发生,因此抑制hNE是一种很有前途的疾病治疗策略。本文简要介绍了hNE的结构、作用机制、生理功能及hNE抑制剂的研发现状,以期能为相关研究提供参考。     

银杏内酯B抑制中性粒细胞活化的研究

目的 研究银杏内酯B(GB,抗血小板聚集)抑制血小板活化因子(PAF)介导的中性粒细胞活化.方法 将银杏内酯B加入抗凝全血中,阻断PAF对中性粒细胞活化;用PAF及二磷酸腺苷(ADP)活化下述各组的中性粒细胞,包括对照组、PAF组、PAF+GB组、ADP组和ADP+GB组,用流式细胞术检测中性粒细胞整和素(CD11b)平均荧光强度.结果 PAF及ADP均可明显增加中性粒细胞CD11b的平均荧光强度,银杏内酯B可明显抑制PAF及ADP诱导的CD11b的平均荧光浓度.结论 银杏内酯B可明显抑制PAF介导的中性粒细胞活化.     

中性粒细胞在组织修复中的作用

传统的观念认为中性粒细胞 (neutrophils,Neu)是一分化终末细胞 ,在伤口仅仅行使杀菌、清理坏死组织的功能。近年来的研究表明 ,Neu还可分泌诸多重要的细胞因子 ,如IL 1,TNF α ,VEGF等 ,参与激活表皮细胞、成纤维细胞、血管内皮细胞 ,启动组织修复 ,并促进呼吸道上皮、角膜上皮增殖、修复。Neu在创面行使正常功能对组织修复的正常进行至关重要     

中性粒细胞缺乏症的护理

中性粒细胞缺乏症(粒缺)是指外周血中性粒细胞绝对值＜0.5×109/L,是血液系统中的"急症".既往治疗方法有限,因继发感染病死率可达70%～90%.目前由于新一代抗生素的应用、成分输血、细胞因子及层流病房的使用,病死率大大降低.     

中性粒细胞胞外陷阱在脑梗死发病机制中的研究进展

中性粒细胞胞外陷阱是由中性粒细胞释放到外周而发挥作用的一种复合物。人们在脑梗死患者的血栓中发现了中性粒细胞细胞外陷阱,并发现中性粒细胞细胞外陷阱与动脉粥样硬化、血栓形成密切相关。中性粒细胞细胞外陷阱可以降低动脉粥样硬化斑块的稳定性,促进血栓的形成,影响梗死后新生血管的生成,中性粒细胞细胞外陷阱还与溶栓后的出血相关,不同类型脑梗死中中性粒细胞细胞外陷阱的分布也存在差异,并且在中性粒细胞细胞外陷阱中发现了炎性小体相关成分,这些都表明中性粒细胞细胞外陷阱在脑梗死发病机制中发挥着重要作用。因此就中性粒细胞细胞外陷阱在脑梗死发病机制中的作用进行综述,主要总结了中性粒细胞细胞外陷阱在动脉粥样硬化、血栓形成、脑梗死后溶栓中的作用以及对脑梗死后新生血管、不同类型脑梗死以及通过炎性小体对脑梗死的影响。     

中性粒细胞激活蛋白-2在大鼠哮喘中性粒细胞中的表达及意义

目的：观察大鼠哮喘中性粒细胞激活蛋白-2（NAP-2）蛋白在中性粒细胞（NEU）上的表达及地塞米松对其的影响,探讨NEU参与哮喘发病的可能作用机制。方法：采用大鼠哮喘模型,随机分成哮喘组、对照组、地塞米松治疗组,分离纯化血NEU,免疫组织化学法测定支气管和血NEU中NAP-2蛋白的表达水平。结果：哮喘组NEUNAP-2蛋白的平均光密度值（0.198±0.016）显著高于对照组值（0.079±0.015）（P〈0.01）;地塞米松治疗组的NEUNAP-2蛋白的平均光密度值（0.135±0.021）显著低于哮喘组且高于对照组（P〈0.01）。哮喘组支气管NAP-2蛋白的平均光密度值（0.226±0.050）显著高于对照组值（0.140±0.012）（P〈0.01）;地塞米松治疗组的支气管NAP-2蛋白的平均光密度值（0.175±0.028）显著低于哮喘组且高于对照组（P〈0.01或P〈0.05）。NEUNAP-2蛋白的表达水平与支气管肺泡灌洗液NEU计数呈显著正相关（n=29,r=0.334,P〈0.05）。结论：哮喘大鼠NEUNAP-2蛋白的表达水平增加,NEU可能通过NAP-2参与哮喘发病的炎症过程;地塞米松部分通过抑制NEUNAP-2的表达从而减轻气道炎症,NAP-2可能与NEU在肺组织中聚集有关。     

氯胺酮抑制人离体中性粒细胞释放超氧阴离子的机制

目的研究氯胺酮的异构体S(+)氯胺酮[S(+)-Ket]和R(-)氯胺酮[R(-)-Ket]对中性粒细胞释放超氧阴离子的影响及机制。方法细胞色素C还原法测定3种刺激剂介导的中性粒细胞超氧阴离子释放量。用荧光分光法检测中性粒细胞内钙的水平。用Western Blot法检测中性粒细胞蛋白质p47phox磷酸化水平。结果S(+)-Ket和R(-)-Ket可抑制N-甲酰甲硫氨酰-亮氨酰-苯丙氨酸(N-formyl-methionyl-leucyl-phenylalanine,fMLP)介导的中性粒细胞释放超氧阴离子(P<0.01)。S(+)-Ket可抑制佛波豆蔻醚乙酸盐(phorbol12-myristate13-acetate,PMA)介导的中性粒细胞释放超氧阴离子和钙离子的增加,而R(-)-Ket可轻度增加PMA介导的中性粒细胞释放超氧阴离子和促进钙离子的增加。S(+)-Ket抑制PMA介导中性粒细胞蛋白质p47phox磷酸化,而R(-)-Ket增强上述作用;钙螯合剂EGTA可取消R(-)-Ket对PMA介导中性粒细胞蛋白质p47phox磷酸化的抑制作用。结论S(+)-Ket通过PKC-钙信息通道,抑制NADPH氧化酶p47phox,抑制超氧阴离子的产生。     

中性粒细胞在急性痛风性关节炎中的作用

痛风是尿酸钠晶体(MSU)沉积于组织或器官引起的一组临床综合征.急性痛风性关节炎(AGA)是痛风发作最典型的时期.中性粒细胞是AGA发作时滑液中主要的细胞群,它通过募集、激活、凋亡、中性粒细胞细胞外网状陷阱形成以及自噬等,在炎症反应的发作和消退阶段起着关键作用.本文综述中性粒细胞在MSU诱导的AGA炎症反应中的作用,进一步了解AGA炎症的发病机制,为AGA的靶向治疗和预防提供理论依据和思路.     

Purines and neutrophil leukocytes

• 1.1. Adenosine is a normal constituent of all body fluids and its levels are raised, for example, by hypoxia and ischemia. In addition, both adenosine and ATP can be released by endothelial cells and neutrophils in response to physiologic stimulation.
• 2.2. Human neutrophil leukocytes possess multiple adenosine receptors and P₂ purinoceptors.
• 3.3. ATP can increase intracellular Ca²⁺ levels in neutrophils, cause degranulation and enzyme release, potentiate the oxidative burst and enhance their adhesion to the endothelium. ATP is broken down to adenosine by ecto-enzymes. Via A₁ receptors, adenosine can increase neutrophil chemotaxis and, via A_2A receptors, it can decrease the oxidative burst, degranulation and adhesion to endothelium.
• 4.4. Adenosine and adenine nucleotides are important endogenous modulators of neutrophil functions, and drugs may exert important actions via purinoceptors on neutrophil leukocytes.

     

促肝细胞生长素对H2O2损伤人LO2细胞的保护作用和机制探究

目的 研究促肝细胞生长素(PHGF)对H2O2损伤LO2细胞的保护作用和机制,为其临床应用提供理论依据.方法 采用MTT法检测PHGF对正常LO2细胞的影响,以考察其细胞毒性.并采用过氧化氢(H2O2)制造LO2细胞体外损伤模型,研究PHGF对H2O2损伤的LO2细胞的保护作用和机制.试验分为5组.空白对照组,H2O2组和三个PHGF浓度组(50、100、200μg·mL-1).采用MTT法检测PHGF对不同组别LO2细胞存活率的影响;运用Western blot法检测各组LO2细胞内目标蛋白的表达情况.结果 PHGF对正常LO2细胞在一定的浓度范围内(500~2.5μg·mL-1)无明显增殖作用也无明显细胞毒作用,通过实验表明,H2O2对LO2细胞造模的最佳浓度为0.25mmol·L-1;PHGF对H2O2诱导的LO2细胞损伤MTT试验结果表明,各浓度组光密度值显著高于H2O2组(P<0.05);Western blot实验表明:PHGF各浓度组,按浓度从高到低,Bcl-2蛋白的表达明显高于H2O2组(WTBXP<0.01),而Bax蛋白的表达明显低于H2O2组(P<0.01).结论 PHGF对H2O2损伤的人LO2细胞具有一定的保护作用,可能与其增强Bcl-2蛋白的表达以及抑制Bax蛋白的表达有关.     

Mechanism underlying H2O2-induced inhibition of acetylcholine-induced contraction in rabbit tracheal smooth muscle

The mechanism underlying the inhibition by H2O2 of acetylcholine-induced contraction was investigated in epithelium-denuded strips of rabbit trachea. Acetylcholine (10 microM) generated a phasic, followed by a tonic increase in both the intracellular Ca2+ concentration ([Ca2+]i) and force. Although the acetylcholine-induced tonic contraction was around 9 times the high K+ (80 mM)-induced one, the two stimulants induced similar [Ca2+]i increases (around 0.2 microM), indicating that acetylcholine generates tonic contraction via increases in both [Ca2+]i and myofilament Ca2+-sensitivity. H2O2 (30 microM) (a) enhanced the acetylcholine-induced tonic (not phasic) increase in [Ca2+]i but attenuated both phases of the acetylcholine-induced contraction and (b) enhanced the high K+-induced increase in [Ca2+]i but did not modify the high K+-induced contraction. In beta-escin-skinned strips, application of acetylcholine in the presence of GTP enhanced the contraction induced by 0.3 microM Ca2+ so that its amplitude became similar to that induced by 1 microM Ca2+. H2O2 (30 microM) attenuated the contraction induced by 0.3 microM Ca2+ (alone or in the presence of acetylcholine) but not those induced by higher concentrations of Ca2+ alone (0.5 microM and 1 microM). These results indicate that H2O2 acts directly on contractile proteins in rabbit tracheal smooth muscle to inhibit the contraction induced by low concentrations of Ca2+ (<0.5 microM). An action of H2O2 that increases [Ca2+]i (and thereby masks this reactive-oxygen-induced inhibition of myofilament Ca2+-sensitivity) is apparent in the presence of high K+ but not of acetylcholine. Thus, in rabbit tracheal smooth muscle H2O2 downregulates myofilament Ca2+-sensitivity more potently during acetylcholine-induced contraction than during high-K+-induced contraction, leading to an effective inhibition of the former contraction.     

Inhibition of active oxygen generation by dipyridamole in human polymorphonuclear leukocytes.

The effect of dipyridamole on active oxygen generation by human polymorphonuclear leukocytes (PMN) was investigated. Dipyridamole inhibited the production of oxidative metabolites from human PMN stimulated by opsonized zymosan and formyl-methionyl-leucyl-phenylalanine dose and time dependently. To determine whether dipyridamole directly inhibits the production of oxygen metabolites by human PMN, human PMN were preincubated with dipyridamole washed prior to stimulation. Dipyridamole was found to directly inhibit human PMN from generated active oxygen metabolites at therapeutic concentrations. Dipyridamole may possibly be a potential scavenger of active oxygen metabolites since it inhibited active oxygen metabolite production from human PMN very rapidly. Dipyridamole was also found to directly affect the scavenging of active oxygen metabolites generated by opsonized zymosan-stimulated human PMN at therapeutic concentrations. This action of dipyridamole was also noted to be exerted against hydroxyl radicals and superoxide anions produced biochemically by an electron spin resonance spectrometer. It thus follows that dipyridamole may inhibit human PMN active oxygen metabolite generation and affect directly the scavenging of active oxygen metabolites at therapeutic concentrations.     

N－（4＇－羧苯基）－4－羟基－3，5－二叔丁基苯甲酰胺对十四烷酰佛波醋酸酯刺激大鼠多形核白细胞生成过氧化氢的影响

Ｎ－（４＇－羧苯基）－４－羟基－３，５－二叔丁基苯甲酰胺对十四烷酰佛波醋酸酯刺激大鼠多形核白细胞生成过氧化氢的影响孙士勇，韩锐（中国医学科学院药物研究所，北京１０００５０）新维甲类化合物Ｎ（４＇－羧苯基）－４－羟基－３，５－二叔丁基苯甲酰胺［Ｎ－（４...     

A proline-rich polypeptide complex (PRP) isolated from ovine colostrum. Modulation of H2O2 and cytokine induction in human leukocytes

A proline-rich polypeptide complex (PRP) has immunoregulatory properties and also shows beneficial effects in Alzheimer's disease (AD). It is known that the unregulated activation of microglial cells in AD may result in chronic inflammatory response. There is a link between the activation of immune cells on the periphery and in the central nervous system (CNS). Therefore, we studied the effect of the PRP on human peripheral blood mononuclear cells (PBMCs) stimulated by LPS with PHA (LP) or PMA as proinflammatory activators. PRP and its nonapeptide fragment (NP) inhibited by 40-60% production of H(2)O(2) induced by PMA. The peptides also inhibited activity of superoxide dismutase. Both peptide preparations showed differential effects on the secretion of cytokines. NP induced TNF-alpha only while PRP induced IL-6, IL-10 and TNF-alpha. On the other hand, the release of TNF-alpha and IL-10 induced by LP in PBMCs was inhibited by PRP while NP inhibited the release of IFN-gamma and IL-10. The results obtained showed that PRP may affect not only adaptive immunity but also innate immunity and thus may regulate secretions of mediators of inflammation. The regulatory effect of the PRP on the innate immunity may shed some light on understanding the beneficial effects of this polypeptide complex in AD patients.     

2,3-吲哚醌对多巴胺能细胞氧化损伤的保护作用

目的采用过氧化氢(H2O2)作为损伤因素,检测2,3-吲哚醌(isatin,ISA)对MES 23.5细胞的保护作用及其机制。方法 MTT比色法检测H2O2的毒性作用及ISA的保护作用。细胞分为:对照组,H2O2 20μmol.L-1组,和ISA 100μmol.L-1+H2O2 20μmol.L-1组,采用流式细胞技术(FCM)检测线粒体膜电位(△ψm)的变化;激光扫描共聚焦显微镜(LSCM)检测细胞内Ca2+浓度([Ca2+]i)变化。结果 H2O2组细胞存活率明细降低。ISA 100μmol.L-1及以上浓度处理的细胞存活率均高于H2O2组(P<0.05)。H2O2组细胞内R123平均荧光强度较对照组明显降低而ISA组明显增强(P<0.01)。H2O2组细胞内Fluo-3荧光强度明显高于对照组(P<0.01),而ISA组细胞内荧光强度明显低于H2O2组(P<0.01)。结论 ISA可减轻H2O2导致的DA能MES 23.5细胞损伤,其机制与减轻△ψm异常,降低[Ca2+]i水平有关。     

过氧化氢熏蒸消毒手术物品的效果观察

本文报道使用过氧化氢熏蒸消毒法用于手术物品的消毒效果。选择电刀导线、尿管、剪刀及橡胶管作为试验对象,将以上物品放于自制的消毒箱内,将过氧化氢加热挥发,封闭消毒箱2h,以上物品消毒前后分别在无菌技术下用同样的方法采集标本,进行细菌培养。结果：消毒后全部无细菌生长,合格率达100%。文章认为,过氧化氢主要是由于加热后挥发释放出新生态氧,破坏细菌酶的结构,致使细菌代谢发生障碍,从而起到杀菌消毒作用。