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1.
糖皮质激素对肿瘤坏死因子引起的大鼠中性粒细胞粘附的影响 总被引:2,自引:0,他引:2
采用中性粒细胞与玻璃珠粘附和PMN与血管内皮细胞粘附两种模型,以肿瘤坏死因子,作为PMN的刺激因子,研究糖皮质激素对TNF引起的大量PMN粘附的影响,同时给予糖皮质激素受体阻断剂RU38486观察GR在粘附中的作用,结果发现,TNF能明显增强大鼠PMN的粘剂;Dex不能抑制经TNF预处理的PMN的粘附(P>0.05),但有一定的预防作用;经TNF预处理再同时给予Dex和RU38486的PMN粘附同 相似文献
2.
我们以糖皮质激素受体(GR)的竞争性拮抗剂RU38486(简称RU486)阻断大鼠体内的GR,并通过检测肺、肾组织匀浆中荧光标记白蛋白的含量,观察了烫伤后12h大鼠肺、肾血管壁通透性的变化以及阻断GR对这种变化的影响。结果显示:烫伤后12h,大鼠肺、肾组织匀浆中荧光标记白蛋白含量明显高于对照组(肺:P<0.05;肾:P<0.001);阻断GR后再烫伤大鼠,其肺、肾组织匀浆中的荧光白蛋白含量又显著高于烫伤组(P<0.05)。提示:①烫伤后12h,大鼠肺、肾血管壁通透性明显升高。②GR减少可加重烫伤所致的血管壁通透性升高,并可逆转内源性糖皮质激素(GC)稳定血管壁通透性的作用。 相似文献
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糖皮质激素受体阻断对烫伤大鼠肺‘肾血管壁通透性变化… 总被引:2,自引:0,他引:2
我们以糖皮质激素受体的竞争性拮抗剂RU38486?(简称RU486)阻断大鼠体内的GR,并通过检测肺、肾组织匀浆中荧光标记白蛋白的含量,观察了烫后12h大鼠肺、肾血管壁通透性的变化以及阻断GR对这种变化的影响。结果显示:烫伤后12h,大鼠肺、肾组织匀浆中荧光标记白蛋白含量明显高于对照组(肺:P<0.05;肾:P<0.001);阻断GR后再烫伤大鼠,其肺、肾组织均浆中的荧光白蛋白含量又显著高于烫伤组 相似文献
4.
慢性肾衰患者血红蛋白浓度变化对血清细胞因子活性的影响作用 总被引:1,自引:0,他引:1
目的为了探讨贫血与慢性肾衰(CRF)免疫功能状态的关系。方法检测了CRF患者单纯输血及用红细胞生成素(EPO)治疗前后细胞因子白细胞介素2(IL2)、可溶性白细胞介素2受体(sIL2R)、肿瘤坏死因子(TNF)及γ干扰素(γIFN)水平,并与肾功能正常肾小球肾炎患者(GN)组及对照组(C)进行比较分析。结果CRF组血清IL2,TNF和γIFN水平均显著低于GN组及C组(P<001),sIL2R水平则较GN组及C组明显升高(P<001)。CRF组血清IL2,TNF和γIFN水平与血红蛋白浓度存在直线正相关,而sIL2R水平与血红蛋白浓度呈负相关性,单纯输血或应用EPO治疗能改变这些细胞因子活性水平。结论CRF免疫功能低下与贫血有关,及时治疗和改善贫血状态可部分纠正这种免疫异常。 相似文献
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小儿肾脏疾病血,尿内皮素的变化 总被引:9,自引:0,他引:9
目的研究小儿肾脏疾病血、尿内皮素(PET、UET)的水平及其相互关系。方法采用同位素放免方法检测了肾病综合征(NS),肾小球肾炎(GN),肾功能衰竭(RF)共72例患儿血及尿中ET,血心钠素(ANP)水平。结果NS,GN,RF三组的PET及UET值明显高于对照组,尤其RF组(P<005,P<0.01)。ANP值在GN组和RF组明显高于对照组(P<001)。8例ARF患儿恢复期血ET水平下降,6例CRF患儿虽经治疗,但血ET水平不降或上升。结论ET在小儿肾脏疾病发病机理及病情进展中可能起重要作用,其值高低与病情严重程度及预后有关。 相似文献
7.
地塞米松对创伤性急性肺损伤家兔肿瘤坏死因子-α的干预作用 总被引:2,自引:0,他引:2
目的 探讨地塞米松(Dex)对创伤性急性肺损伤(ALI)治疗作用的可能机制。方法 采用逆转录聚合酶链反应(RT-PCR)、酶联免疫吸附法(ELISA)检测24只大耳白兔肺组织肿瘤坏死因子-α基因(TNF-αmRNA)表达及肺泡巨噬细胞(AM)培养上清液中肿瘤坏死因子-α(TNF-α)、白细胞介素(IL)-6水平。结果 创伤性ALI兔肺组织TNF-αmRNA表达及AM培养上清液中TNF-α,IL-6含量较正常对照组比较明显升高(P〈0.01)。Dex治疗后能显著下调TNF-αmRNA的表达(68%,P〈0.01),降低AM分泌TNF-α(P〈0.05)及IL-6水平(P〈0.01)。结论 Dex能缓解创伤性ALI的发生、发展。其机制与其对TNF-α、IL-6等炎性介质的调节作用密切相关。 相似文献
8.
生长因子对间皮细胞增殖及合成细胞外基质的影响 总被引:1,自引:0,他引:1
目的 探讨血小板源生长因子bb(PDGFbb) 、转化生长因子β(TGFβ) 对人腹膜间皮细胞(HPMC)增殖及合成细胞外基质(ECM) 的影响。方法 建立HPMC体外培养体系。3HTdR 掺入法测定细胞增殖;放射免疫法检测细胞上清中Ⅲ型前胶原( ⅢPC) 。结果 PDGFbb 促进、但TGFβ抑制HPMC增殖,均呈剂量依赖性( P< 0-01) 。2 者均能刺激HPMC 产生ⅢPC( P< 0-01)。结论 CAPD相关性腹膜炎时腹腔中高浓度的PDGFbb 、TGFβ能调节间皮层的修复和重塑,刺激其合成分泌ECM,后者可能是腹膜炎(PI)反复发生最终导致腹膜硬化的重要机制之一。 相似文献
9.
目的 探讨肿瘤坏死因子抗膀胱癌细胞作用的影响因素。方法 将肿瘤坏死因子α(TNF-α)和不同浓度的丝裂霉素(MC),顺铂(CDDP)以及干扰素α(IFN-α)作用于体外培养的膀胱癌细胞系BIU-87,用噻唑蓝(MTT)法测定细胞毒效果。结果 TNF-α对BIU-87细胞有明显的浓度依赖性抑制作用,MC(2.5~5.0mg/L)或IFN-α(2500U-5000U/ml)与TNF-α(10000U/ 相似文献
10.
为探讨NIDDM患者Fn、PAG改变与缺血性心脑血管病的关系,分析53例NIDDM患者Fu、PAG测定结果,并与53名健康人比较。患者组Fn明显高于(P〈0.01),前者PAG(1)、MAR、I与后者有显著统计学差异(P〈0.01)。患者组中并发症组与无并发症组Fn、I较对照组有明显统计学差异(P〈0.01),并发症组PAG(1)、MAR明显高于对照组(P〈0.05)。NIDDM患者Fn降低、PA 相似文献
11.
采用中性粒细胞(PMN)与玻璃珠粘附和PMN与血管内皮细胞(EC)粘附两种模型,以肿瘤坏死因子(TNF),作为PMN的刺激因子,研究糖皮质激素(GC)对TNF引起的大鼠PMN粘附的影响,同时给予糖皮质激素受体(GR)阻断剂RU38486观察GR在粘附中的作用。结果发现,TNF能明显增强大鼠PMN的粘附(P<0.01);Dex不能抑制经TNF预处理的PMN的粘附(P>0.05),但有一定的预防作用;经TNF预处理再同时给予Dex和RU38486的PMN粘附同样明显增强(P<0.01)。 相似文献
12.
Tumor necrosis factor-enhanced leukotriene B4 generation and chemotaxis in human neutrophils 总被引:2,自引:0,他引:2
J D Meyer R W Yurt R Duhaney D G Hesse K J Tracey Y M Fong M Verma G T Shires P Dineen S F Lowry 《Archives of surgery (Chicago, Ill. : 1960)》1988,123(12):1454-1458
In an in vivo study of five normal volunteers infused with endotoxin (20 U/kg of US reference endotoxin lot EC-5), increased neutrophil (PMN) generation of leukotriene B4 and chemotaxis to leukotriene B4 were found concomitantly with elevated plasma tumor necrosis factor (TNF) levels. To clarify the role of TNF in PMN activation, neutrophil responsiveness after in vitro treatment with TNF was examined. Neutrophils from seven normal subjects were incubated with TNF for 30 minutes and tested for chemotaxis to leukotriene B4, formyl-methionyl-leucyl-phenylalanine and zymosan-activated serum, or the calcium ionophore A23187 to assess leukotriene B4 generation. A range of 10(-13) to 10(-9) mol/L of TNF was used for these assays. When 10(-9) mol/L of TNF was used, the amount of leukotriene B4 that was produced was significantly greater than in control cells. The effect of TNF on PMN chemotaxis was uniformly inhibitory for the three stimuli at 10(-10) mol/L compared with untreated cells. At a picomolar range, PMN migration to leukotriene B4, but not to zymosan-activated serum or formyl-methionyl-leucyl-phenylalanine, was significantly increased over that of PMNs not exposed to TNF. This suggests that TNF has a specific facilitatory effect on PMN responsiveness for both leukotriene B4 production and chemotaxis to leukotriene B4 and may be the same signal for this phenomenon in endotoxemic patients. 相似文献
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C J Walsh S K Leeper-Woodford P D Carey D J Cook D E Bechard A A Fowler H J Sugerman 《The Journal of surgical research》1991,50(4):323-329
Sequestration of neutrophils (PMNs) in the pulmonary microvasculature and associated neutropenia are characteristic features of experimental models of septic lung injury. The etiology of altered PMN kinetics during septic lung injury is uncertain, but may be partially due to increased adhesiveness of activated PMNs to pulmonary endothelium. This study examines the relationship between the expression of PMN CD18 adhesion receptors, the evolving neutropenia, and plasma tumor necrosis factor (TNF) activity in a porcine model of septic lung injury. Acute lung injury was induced by infusion of live Pseudomonas aeruginosa (5 x 10(8) CFU/ml at 0.3 ml/20 kg/min) for 60 min (Group Ps, n = 6). Control animals (Group C, n = 3) received a 60-min infusion of sterile 0.9% saline. CD18 expression of circulating PMNs was measured by quantitative immunofluorescent flow cytometry. Plasma TNF activity was measured by L929 fibroblast cytolytic assay. Group Ps developed a significant neutropenia by 30 min (14.9 +/- 2.5 vs 23.4 +/- 3.3 x 10(3) cells/microliter at baseline, P less than 0.05, ANOVA) with circulating neutrophils exhibiting significantly increased CD18 expression by 60 min (6.34 +/- 0.72 vs 5.01 +/- 0.52 equivalent soluble fluorescence molecules (ESFM) x 10(3) at baseline, P less than 0.05, ANOVA). Group Ps demonstrated a significant increase in plasma TNF activity by 30 min (2.5 +/- 0.9 vs 0.7 +/- 0.3 U/ml at baseline). There was no significant change in PMN count, PMN CD18 expression, or plasma TNF activity in Group C. In complimentary in vitro studies, porcine PMNs stimulated with recombinant human TNF-alpha (n = 5) demonstrated a time- and dose-dependent increase in CD18 expression.(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
15.
Levente Pócs Ágnes Janovszky Dénes Garab Gabriella Terhes Imre Ocsovszki József Kaszaki Mihály Boros József Piffkó Andrea Szabó 《Journal of orthopaedic research》2018,36(1):97-105
16.
Cytokines enhance the production of a chemotactic factor for polymorphonuclear leukocytes by rat renal glomerular epithelioid cells 总被引:3,自引:0,他引:3
Human recombinant interleukin-1 beta (IL-1) and tumor necrosis factor-alpha (TNF) dose-dependently enhanced the production of PMN chemotactic factor, which was trypsin-sensitive and heat-stable, by the epithelioid cells of rat renal glomeruli. Dexamethasone dose-dependently suppressed the chemoattractant production. Molecular weight and isoelectric point of this factor were 10 kDa and over 10, respectively. These results suggest that PMN migration to glomeruli occurs without participation of complement system when TNF or/and IL-1 are produced by activated cells in glomeruli. 相似文献
17.
烧伤后白细胞与内皮细胞粘附分子介导作用的研究 总被引:3,自引:0,他引:3
为研究白细胞粘附依赖于细胞粘附分子的介导作用,作者通过离体实验观察分析了烧伤血清对外周血中性粒细胞(PMN)CD11b/CD18表达的影响及CD11b/CD18在烧伤后PMN粘附中的介导作用。结果表明:(1)烧伤血清使PMNCD11b/CD18分子表达和PMN与肺微血管内皮细胞(PMEC)的粘附率增高。(2)CD11b/CD18单抗不仅能使正常PMN与PMEC的粘附率下降50%,也使烧伤血清激活的PMN与PMEC粘附率下降至烧伤血清激活前水平。我们认为,严重烧伤能使外周血PMNCD11b/CD18表达明显增高,CD11b/CD18不但介导基础状态下的PMN粘附,更是介导烧伤后引起的大量PMN与PMEC粘附的主要分子。 相似文献
18.
烟雾吸入伤血清对中性粒细胞粘附及迁移作用的体外研究 总被引:1,自引:0,他引:1
目的 通过鼠烟雾吸入伤血清体外刺激培养内皮细胞和中性粒细胞(PMN),了解PMN粘会与迁移变化,以及抗CD11a,抗CD11b和抗ICAM-1对PMN粘附与迁移的影响,探讨粘附因子在烟雾吸入性损伤中的作用。方法 在体外实验中用荧光标记PMN,测定PMN与烟雾吸入性损伤血清刺激的内皮细胞的粘附率,在5μm滤膜上培养仙皮细胞测定PMN迁移量,并采用抗体阻断技术,测定了粘附因子CD11a,CD11b和I 相似文献
19.
烧伤后粘附分子介导中性粒细胞粘附对肺血管通透性的影响 总被引:4,自引:0,他引:4
目的观察比较烧伤血清及烧伤后中性白细胞(PMN)对肺血管通透性的影响,分析PMN粘附及粘附分子CD11b/CD18在该影响中的介导作用。方法应用离体肺灌流技术,通过肺重量增加(LWG)、液体滤过系数(Kf)和通透性表面积乘积(PS)分别观察肺水肿程度、肺血管对小分子物质和大分子物质的通透性。结果烧伤血清能使LWG、Kf和PS明显增加,以Kf增加最为明显;烧伤后PMN也能使Kf和PS增加,以PS增加为明显;用单抗封闭烧伤后PMN膜上CD11b/CD18后,PMN在肺血管内的滞留减少,Kf和PS值增加被抑制,并以PS改变为显著。结论(1)被激活的PMN释放的介质类物质如氧自由基、蛋白酶等物质对肺微血管内皮细胞(PMEC)的损伤作用部分依赖于PMN与内皮细胞的粘附。(2)烧伤后被激活的PMN释放的介质类物质主要介导肺血管对小分子物质通透性的影响。烧伤后PMN与肺微血管内皮细胞(PMEC)的粘附除了使介质类物质的作用放大外,还介导肺血管对大分子物质通透作用。(3)PMN膜上CD11b/CD18分子可能通过与PMEC细胞间粘附分子的结合,本身具有对内皮细胞的生物学调控作用 相似文献
20.
Alterations in immunocyte tumor necrosis factor receptor and apoptosis in patients with congestive heart failure 总被引:5,自引:0,他引:5
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Rumalla VK Calvano SE Spotnitz AJ Krause TJ Hilkert RJ Lin E Lowry SF 《Annals of surgery》2002,236(2):254-260
OBJECTIVE: To examine systemic immune cell proinflammatory receptor expression and apoptosis in patients with congestive heart failure (CHF). SUMMARY BACKGROUND DATA: Prior studies have demonstrated that CHF is associated with a chronic myocardial inflammatory state, including increased plasma proinflammatory cytokine and soluble receptor expression. By contrast, it has also been shown that tumor necrosis factor (TNF) receptor protein expression is decreased in the failing myocardium. However, no studies to date have examined systemic immune cell proinflammatory receptor expression or function as disease markers in patients with heart failure. METHODS: Twenty-nine patients were studied prospectively over an 8-month period at a single institution. One group (n = 16) had a history of clinical symptoms of CHF and moderate to severe left ventricular dysfunction. The second group (n = 13) consisted of patients who had coronary artery disease without symptoms of CHF and documented preservation of left ventricular function. Blood samples were analyzed for polymorphonuclear cell (PMN) and monocyte TNF and CD95 membrane-associated receptor expression, spontaneous and CD95 (Fas)-mediated PMN apoptosis, and plasma cytokine and soluble TNF receptor levels. Isolated PMNs were incubated for 6 hours with or without CH 11, a CD95 agonist. Propidium iodide/RNAase staining and flow cytometry was used to assess apoptosis, defined as PMNs expressing hypodiploid DNA (<2 n DNA). Membrane-associated TNF receptor and CD95 were also measured by flow cytometry. Plasma levels of TNF, interleukin (IL)-6, IL-10, and soluble TNF receptors 1 and 2 were quantified using enzyme-linked immunosorbent assay. RESULTS: Compared to patients without CHF, circulating PMN and monocyte TNF receptor levels were significantly decreased in patients with CHF. By contrast, PMN and monocyte CD95 expression was not significantly changed in patients with CHF versus those without CHF. Patients with CHF had a 60% decrease in spontaneous PMN apoptosis compared to patients without CHF, whereas no significant difference in CD95-mediated apoptosis was observed between the two groups. Pearson-product movement correlation of monocyte TNF receptor expression and spontaneous PMN apoptosis rates versus patients' ejection fraction was performed and was statistically significant. Plasma levels of soluble TNF receptor 2 (p75) were elevated in CHF patients versus patients without CHF, while there was no significant difference in soluble TNF receptor 1 (p55), TNF, IL-6, and IL-10 between the two groups. CONCLUSIONS: These data demonstrate a systemic alteration in immune cell phenotype and apoptosis in patients with CHF. These findings provide support for the concept that inflammatory mediators either contribute to myocardial dysfunction or are elaborated systemically by left ventricular compromise. This present study suggests that immune cell TNF receptor expression and diminished PMN apoptosis may serve as biologic markers of myocardial failure. 相似文献