共查询到19条相似文献,搜索用时 109 毫秒
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气道上皮损伤与支气管哮喘 总被引:2,自引:0,他引:2
支气管哮喘发病过程中 ,多种因素可导致气道上皮损伤。损伤的气道上皮细胞通过细胞因子介质与气道平滑肌细胞、成纤维细胞及炎症细胞间的相互作用 ,参与了气道炎症、气道重塑及气道高反应性的形成 ,成为哮喘发病过程的中心环节 相似文献
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<正>Pendrin蛋白是可溶性转运家族26A(SLC26A)中的一员,SLC26A是一个阴离子交换转运体家族,包含SAT-1、DTDST、DRA/CLD及prestin等多个可转运各种阴离子的成员。该蛋白在体内分布广泛,主要功能为转运氯离子、碘离子、碳酸氢根等多种单价或二价离子,从而维持组织中离子的稳态。近年有研究显示pendrin表达于呼吸道上皮,并与支气管哮喘关系密切,这为人们研究哮喘发病机制和找寻 相似文献
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支气管哮喘实验模型的研究进展 总被引:7,自引:0,他引:7
支气管哮喘是一种慢性气道变应性炎症。支气管哮喘实验动物模型的建立在研究其发生发展中具有重要作用。本文概述了近年来支气管哮喘实验动物模型的研究进展,为进一步明确支气管哮喘病因和发病机制,制定治疗方案提供研究手段。 相似文献
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过氧亚硝基阴离子在哮喘豚鼠气道高反应性中的作用 总被引:10,自引:0,他引:10
目的 探讨哮喘豚鼠内过氧亚硝基阴离子(ONNOO^-)的生成及其在哮喘气道高反应性形成中的作用。方法 18只哮喘豚鼠模型随机分为3组:(1)哮喘组(6只):用10%卵蛋白1ml腹腔注射液致敏,2周后用1%卵蛋白超声雾化吸入复制豚鼠哮喘模型。(2)哮喘加氨基胍(AG)组(6只):该喘同哮喘组,在每次诱喘前1h腹腔注射AG10mg/kg。(3)正常对照组(6只):用生理盐水代替诱喘剂。每组哮喘豚鼠均用 相似文献
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支气管哮喘(哮喘)动物实验模型对哮喘的发病原因、诱发因素、发病机制、药物防治等的研究起到了在动作用。本文概述了变应原、变应性炎症中间产物、生物因素、物理因素等诱发的动物实验性哮喘及其发生机制,以及各个模型的优缺点,研究者可根据研究目的选择应用。 相似文献
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支气管哮喘(简称哮喘)是一种由多细胞,多细胞组分参与形成的慢性气道炎症性疾病。支气管上皮细胞是气道结构细胞作为抵抗外界损伤因素的第一道防线,当吸入性刺激物质时,首先激化支气管上皮细胞并破坏上皮细胞的正常结构和生理功能,应激状态下的上皮细胞通过分泌炎性介质与自身细胞或其他气道结构细胞、炎性细胞、抗原递呈细胞等相互作用,积极参与哮喘的气道慢性炎症发生与发展进程。 相似文献
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支气管哮喘动物实验模型的研究现状 总被引:8,自引:1,他引:7
陈颖 《国外医学:呼吸系统分册》2000,20(3):154-156
支气管哮喘(哮喘)动物实验模型对哮喘的发病原因、诱发因素、发病机制、药物防治等的研究起到了推动作用。本概述了变应原、变应性炎症中间产物、生物因素、物理因素等诱发的动物实验性哮喘及其发生机制,以及各个模型的优缺点,研究可根据研究目的选择应用。 相似文献
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支气管哮喘(简称哮喘)是一种由多种细胞、多种细胞因子参与形成的慢性气道炎症性疾病.气道上皮细胞是气道结构细胞,在应激状态下的上皮细胞通过分泌炎性介质与自身细胞或其他气道结构细胞、炎性细胞、抗原递呈细胞等相互作用,积极参与哮喘的发生、发展.阐明维持气道上皮正常结构和功能的分子机制,可能在未来哮喘防治中占有重要意义.本文综述气道上皮在哮喘发生、发展中的作用及相关机制的研究进展. 相似文献
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豚鼠哮喘模型气道上皮细胞原癌基因c—fos表达的研究 总被引:1,自引:0,他引:1
豚鼠哮喘模型气道上皮细胞原癌基因c┐fos表达的研究戚好文刘振千薛辉哮喘是一种气道慢性变态反应性疾病,在气道炎症的发生过程中,气道内上皮细胞起到了重要作用。与正常细胞相比,上皮细胞呈现活化状态,表达、分泌有关炎症介质[1,2]。上皮细胞的活化可能与原... 相似文献
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支气管哮喘干预措施对气道反应性的影响 总被引:2,自引:0,他引:2
气道高反应性(AHR)是支气管哮喘(哮喘)的重要特点,多种哮喘干预措施可影响气道反应性。吸入糖皮质激素可明显降低AHR,白三烯调节剂降低AHR的作用弱于吸入糖皮质激素。吸入短效β2受体激动剂对AHR有不利影响,而长效β2受体激动剂对AHR无明显影响。避免过敏原能明显改善职业性哮喘患者的AHR。某些免疫治疗方法可减轻部分哮喘患者的AHR。 相似文献
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Gail M. Brottman Warren E. Regelmann Arne Slungaard O. Douglas Wangensteen 《Pediatric pulmonology》1996,21(3):159-166
Increased numbers of eosinophils and increased concentrations of plasma proteins have been found in the airways of patients with mild asthma. We used an intact guinea pig trachea model to investigate the role of eosinophil peroxidase (EPO) in altering the function of the airway epithelial barrier, EPO in the presence of hydrogen peroxide (H2O2) and bromide (Br−) catalyzes the production of hypobromous acid (HOBr), which is felt to have a toxic effect on airway epithelial cells. An intact guinea pig trachea was mounted on an apparatus in a way that would allow the tracheal epithelium to be exposed to different solutions. Following these exposures, a test solution containing 14C-sucrose (S), 3H-inulin (I), and FITC-dextran-20 (D) was placed in the tracheal lumen and positioned in the center of the segment for 90 minutes. Flux of these molecules across the epithelial barrier into a bath was measured, and the permeability (P) was calculated for each molecule to quantify epithelial barrier function. Light and electron micrographic studies were performed to assess cellular damage. We found that there was a dose response to EPO (in the presence of fixed amounts of H2O2 and Br−). EPO at 7.3 × 10−7 M caused no increase in P over controls (Ringer's solution alone) for S, I, or D (P > 0.05), whereas EPO at 2.7 × 10−6 M caused a significant increase in P over controls (P = 0.008) for all test molecules. Light and electron micrographs of the latter tracheas showed no evidence of microscopic changes despite the increased P. Further testing verified that the increase in permeability was caused by the EPO catalyzed reaction and not the individual substrates themselves, and that the reaction was inhibited by a peroxidase inhibitor. We conclude that EPO can alter the barrier function of the airway epithelium before gross cellular damage becomes visible. We hypothesize that changes in the tight junctions are responsible for the alteration in the barrier function of the airway epithelium and that this may play an important role in the pathophysiology of mild asthma. Pediatr Pulmonol. 1996; 21:159–166. © 1996 Wiley-Liss, Inc. 相似文献
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S. Işık M. Karaman S.Ç. Micili Ş. Çağlayan-Sözmen H.A. Bağrıyanık Z. Arıkan-Ayyıldız N. Uzuner Ö. Karaman 《Allergologia et immunopathologia》2018,46(1):67-75
Background
Sinomenine (SIN), an alkaloid isolated from the root of Sinomenium acutum which has a variety of pharmacological effects, including anti-inflammation, immunosuppression and anti-angiogenesis. The present study aimed to evaluate the effects of SIN on airway remodelling, epithelial apoptosis, and T Helper (Th)-2 derived cytokine levels in a murine model of chronic asthma.Methods
Twenty-two BALB/c mice were divided into four groups; I (control), II (placebo), III, IV. Mice in groups III and IV received the SIN (100 mg/kg), and dexamethasone (1 mg/kg) respectively. Epithelium thickness, sub-epithelial smooth muscle thickness, number of mast and goblet cells of samples isolated from the lung were measured. Immunohistochemical scorings of the lung tissue for matrix metalloproteinase-9 (MMP-9), vascular endothelial growth factor (VEG-F), transforming growth factor-beta (TGF-β), terminal deoxynucleotidyl transferase-mediated dUTP nick endlabeling (TUNEL) and cysteine-dependent aspartate-specific proteases (caspase)-3 were determined. IL-4, IL-5, IL-13, Nitric oxide in bronchoalveolar lavage fluid (BALF) and ovalbumin-specific immunoglobulin (Ig) E in serum were quantified by standard ELISA protocols.Results
The dose of 100 mg/kg SIN treatment provided beneficial effects on all of the histopathological findings of airway remodelling compared to placebo (p < 0.05). All cytokine levels in BALF and serum and immunohistochemical scores were significantly lower in 100 mg/kg SIN treated group compared to the placebo (p < 0.05).Conclusions
These findings suggested that the dose of 100 mg/kg SIN improved all histopathological changes of airway remodelling and its beneficial effects might be related to modulating Th-2 derived cytokines and the inhibition of apoptosis of airway epithelial cells. 相似文献15.
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《Allergologia et immunopathologia》2017,45(4):339-349
Background and aimsIn previous studies, anti-inflammatory, anti-apoptotic and immunomodulatory effects of ursodeoxycholic acid (UDCA) on liver diseases have been shown. In this study, we aimed to investigate the effects of UDCA on airway remodelling, epithelial apoptosis, and T Helper (Th)-2 derived cytokine levels in a murine model of chronic asthma.MethodsTwenty-seven BALB/c mice were divided into five groups; PBS-Control, OVA-Placebo, OVA-50 mg/kg UDCA, OVA-150 mg/kg UDCA, OVA-Dexamethasone. Mice in groups OVA-50 mg/kg UDCA, OVA-150 mg/kg UDCA, OVA-Dexamethasone received the UDCA (50 mg/kg), UDCA (150 mg/kg), and dexamethasone, respectively. Epithelium thickness, sub-epithelial smooth muscle thickness, number of mast and goblet cells of samples isolated from the lung were measured. Immunohistochemical scorings of the lung tissue for matrix metalloproteinase-9 (MMP-9), vascular endothelial growth factor (VEG-F), transforming growth factor-beta (TGF-β), terminal deoxynucleotidyl transferase-mediated dUTP nick endlabeling (TUNEL) and cysteine-dependent aspartate-specific proteases (caspase)-3 were determined. IL-4, IL-5, IL-13, Nitric oxide, ovalbumin-specific immunoglobulin (Ig) E levels were quantified.ResultsThe dose of 150 mg/kg UDCA treatment led to lower epithelial thickness, sub-epithelial smooth muscle thickness, goblet and mast cell numbers compared to placebo. Except for MMP-9 and TUNEL all immunohistochemical scores were similar in both UDCA treated groups and the placebo. All cytokine levels were significantly lower in group IV compared to the placebo.ConclusionsThese findings suggested that the dose of 150 mg/kg UDCA improved all histopathological changes of airway remodelling and its beneficial effects might be related to modulating Th-2 derived cytokines and the inhibition of apoptosis of airway epithelial cells. 相似文献
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目的 探讨支气管哮喘(简称哮喘)患者气道炎症特征及其可能机制,并进一步观察吸入糖皮质激素治疗对气道炎性细胞分类计数、炎症介质等的影响.方法 分别选择轻度(轻度组)、中度(中度组)和重度(重度组)持续哮喘患者15例、14例和19例,正常对照组15名,分别行哮喘症状控制评分、肺功能测定、诱导痰炎性细胞分类计数、调节激活正常T细胞表达和分泌细胞因子(RANTES)、嗜酸粒细胞阳离子蛋白(ECP)、白介素8(IL-8)及髓过氧化物酶(MPO)浓度检测,然后规范吸人糖皮质激素治疗4周,随访复查上述指标.结果 诱导痰NEU%、IL-8及MPO重度组明显升高,分别为(62.40±22.05)%、594.53±85.11、39.25±10.67与轻度组[(47.23±15.12)%、183.63±120.98、12.47±4.15]、中度组[(46.13±19.23)%、352.76±71.72、22.93±7.35]、正常对照组[(31.44±13.31)%、103.26±36.33、10.22±4.13]比较差异均有统计学意义(P<0.01);RANTES、嗜酸粒细胞百分比(EOS%)和ECP浓度在各哮喘组间比较差异无统计学意义(P>0.05).EOS%与RANTES、ECP水平呈正相关(r=0.557,P<0.05;r=0.852,P<0.01);NEU%与IL-8、MPO水平呈正相关(r=0.732,P<0.05;r=0.806,P<0.05);经糖皮质激素治疗后,对轻、中、重度哮喘患者合并进行分析表明,治疗后症状评分由(9.8±5.4)分下降至(4.0±3.5)分和肺功能指标第一秒用力呼气容积占预计值百分比由(62.2±23.3)%升高至(75.9±17.5)%显著改善,差异有统计学意义(P<0.01).在接受糖皮质激素治疗后,RANTES、EOS%和ECP水平均显著降低.另外MPO水平也显著降低(P<0.01);但治疗后在重度组仍显著高于轻、中度组(P<0.01).但IL-8、NEU%治疗后无明显降低(P>0.05),而且治疗后IL-8、NEU%在重度组仍显著高于轻、中度组(P<0.01).结论 中性粒细胞增多是重度哮喘的气道炎症特征之一,EOS与病情严重程度无关.EOS哮喘的发生可能与RANTES的趋化、EOS的活化、ECP的释放有关,激素可以抑制EOS气道炎症.而中性粒细胞哮喘的发生可能与IL-8的趋化、NEU的活化、MPO的释放有关. 相似文献
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Clara细胞蛋白10与哮喘豚鼠气道反应性的相关性研究 总被引:1,自引:0,他引:1
目的观察支气管哮喘豚鼠模型血清和肺匀浆Clara细胞蛋白10(CC10)的CD值变化及其与气道反应性的相关性。方法2004-04-2004-06成都军区昆明总医院呼吸科用10%卵蛋白致敏豚鼠,建立哮喘模型,用生理记录仪测定气道反应性,酶联法检测血清、肺匀浆中的CC10的OD值。结果与正常组比较,哮喘组的血清CC10的OD值差异无显著性(P〉0.05),肺匀浆CC10CD值差异有显著性(P〈0.05);气道反应性与肺匀浆CC10负相关,与血清CC10含量无相关性(P〉0.05)。结论肺组织CC10减少,与气道高反应性呈负相关,提示了CC10可能是一种重要的内源性抗炎保护因子,参与了哮喘的发病。 相似文献
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目的 比较卵清蛋白(ovalbumin,OVA)诱导的急性期和慢性期哮喘小鼠模型在气道炎症、气道重塑和气道高反应方面的差异,明确在哮喘致病过程中肺组织的病理变化.方法 48只BALB/c小鼠随机分为急性组和慢性组,其中急性组包括正常对照组(A1组)和急性哮喘组(A2组),慢性组包括正常对照组(B1组)和慢性哮喘组(B2组).OVA致敏和激发方法分别构建急性早期哮喘模型和慢性期哮喘模型后,测定气道阻力,BALF细胞计数和分类计数,酶联免疫吸附测定(enzyme-linked immunosorbent assay,ELISA)检测IL-4、IL-5、转化生长因子-β1(transforming growth factor-β1,TGF-β1)、血管内皮生长因子(vascular endothelial growth factor,VEGF)和γ-干扰素(interferon-γ,IFN-γ).HE染色观察气道炎症,AB-PAS和Masson染色测定气道重塑.结果 与正常小鼠相比,A2组和B2组小鼠气道阻力均明显升高,但B2组小鼠气道阻力在基础值即发生明显改变.相比于慢性组哮喘小鼠,急性组哮喘小鼠BALF中细胞总数和嗜酸粒细胞数,IL-4、IL-5和IFN-γ水平,肺组织气道血管周围炎症细胞聚集,以及气道黏液分泌水平等炎症性改变更为明显.相比于A2组,B2组哮喘小鼠BALF中TGF-β1和VEGF水平,气道平滑肌增厚,上皮下胶原沉积,上皮下纤维化等改变更为显著.结论 在急性早期哮喘中主要是以炎症性改变为主,但在哮喘早期即开始出现轻度的重塑性改变;而在慢性期哮喘中虽然存在炎症性改变,但影响哮喘症状的因素却主要以器质性改变为主. 相似文献