PTEN在哮喘大鼠气道平滑肌细胞增生中的作用

目的:探讨哮喘大鼠肺组织中PTEN表达的变化及其在气道平滑肌细胞增生中的作用.方法:清洁级雄性Wistar大鼠16只随机分为对照组和哮喘组,每组8只.用卵蛋白(OVA)致敏与激发建立大鼠哮喘模型,末次激发后HE染色法观察哮喘组大鼠支气管-肺组织中炎性细胞浸润情况及气道形态学改变,免疫组化法检测增生细胞核抗原(PCNA)及PTEN蛋白在大鼠肺组织中的表达,RT-PCR法检测肺组织PTEN mRNA表达.结果:哮喘组大鼠气道壁和肺组织中可见大量炎症细胞浸润,气道平滑肌增生肥厚;与对照组比较,哮喘组PCNA蛋白表达显著增强(P < 0.05),PTEN蛋白及其mRNA表达则显著减弱(P < 0.05).结论:PTEN基因失活可能在哮喘气道平滑肌增生中起重要作用,该作用可能与PI3K信号传导通路有关.     

地塞米松对哮喘动物模型支气管平滑肌MLCK表达的影响

目的观察地塞米松(DXM)对哮喘动物模型支气管平滑肌肌球蛋白轻链激酶(MLCK)表达的影响,探讨MLCK在哮喘发病中的作用。方法24只♂SD大鼠,随机等分为正常对照组、哮喘模型组和地塞米松组。以卵蛋白(OVA)诱发大鼠支气管哮喘模型。地塞米松组大鼠于每次激发前1h给予腹腔注射地塞米松0.5mg·kg-1。用免疫组织化学法和免疫印迹法分析三组大鼠支气管平滑肌中MLCK表达。结果免疫组织化学法分析显示DXM组大鼠支气管平滑肌MLCK的表达低于哮喘模型组(P<0.05),但与正常对照组比较差异无显著性(P>0.05)。同时,免疫印迹法检测也表明哮喘模型组大鼠smMLCK表达高于正常对照组及地塞米松组。结论MLCK参与支气管哮喘的发病,地塞米松通过下调哮喘大鼠支气管平滑肌MLCK表达,可能是糖皮质激素治疗哮喘的一种机制。     

1,25-二羟维生素D3对哮喘大鼠维生素D3上调蛋白1的影响

目的探讨1,25-二羟维生素D3(1,25(OH)2D3)对哮喘大鼠维生素D3上调蛋白l(VDUP1)的表达及气道炎症的影响.方法28只Wistar大鼠随机分为四组:对照组、哮喘组、1,25-(OH)2D3组和地塞米松组.以卵蛋白为致敏原制备哮喘大鼠模型,1,25-(OH)2D3组在激发前1h口服1,25-(OH)2D...     

阿托伐他汀对哮喘大鼠气道炎症及气道重构的影响

目的：探讨阿托伐他汀对卵清白蛋白致敏哮喘模型大鼠气道炎症和重构的影响。方法清洁级 SD 雄性大鼠24只按随机数字表法分为对照组、哮喘组和阿托伐他汀组,每组8只。对照组大鼠采用0．9％氯化钠溶液（生理盐水）进行致敏和激发,哮喘组大鼠采用卵清白蛋白致敏和激发,阿托伐他汀组在致敏和激发前以阿托伐他汀口服。采用肺功能检测3组大鼠气道呼气阻力;采用图像分析软件测定肺组织切片中的支气管壁内周长、支气管管壁面积、支气管平滑肌面积;胶原表达通过气道壁 Masson 染色进行观察;实验动物血清中白介素－13（IL－13）及转化生长因子－β1（TGF－β1）的水平以 ELISA 法测定。结果肺功能检测显示哮喘组平均呼气阻力显著升高,阿托伐他汀组低于哮喘模型组（ P ＜0．05）;病理检查显示哮喘组气道炎症明显,对照组和阿托伐他汀组与之相比炎症轻微;阿托伐他汀组大鼠气道管壁面积、平滑肌面积图像分析和哮喘组比较差异有统计学意义（ P ＜0．05）;阿托伐他汀组肺组织中胶原沉积表达较哮喘组减少（ P ＜0．05）;阿托伐他汀组大鼠血清中 IL－13和 TGF－β1较哮喘组降低（ P ＜0．05）。结论阿托伐他汀能够明显减轻哮喘大鼠气道炎症,降低哮喘大鼠的气道基本阻力;减少肺组织中胶原沉积,降低气道管壁面积、平滑肌层面积,减轻哮喘气道重构。阿托伐他汀治疗能够降低血清中 TGF －β1和 IL－13水平,或为其减轻炎症和气道重构的机制。     

加味金匮肾气丸对哮喘大鼠气道炎症的缓解作用及其机制研究

目的 研究加味金匮肾气丸对支气管哮喘大鼠气道炎症的缓解作用及其机制。方法 60只健康大鼠随机分成正常对照组、模型组、地塞米松组、加味金匮肾气丸低、中、高剂量组,以卵白蛋白(OVA)致敏激发制备哮喘模型,观察各组大鼠肺组织病理学的改变,测定肺泡灌洗液中嗜酸性粒细胞(eosinophils,EOS)计数和肺组织中胸腺活化调节趋化因子(thymus activation regulated chemokine,TARC)含量。结果 加味金匮肾气丸能减轻哮喘大鼠模型的喘息症状、降低支气管肺泡灌洗液中EOS计数和肺组织中TARC的含量,结果均有显著性差异(P<0.01或P<0.05)。病理组织学检查结果显示,模型组大鼠肺组织支气管黏膜上皮细胞以及杯状细胞增生,肺泡内有分泌物和炎性细胞浸润,官腔狭窄;各药物组病理改变均显著减轻。结论 加味金匮肾气丸治疗支气管哮喘的机制可能是通过抑制TARC和减少EOS浸润而实现的。     

曲安奈德棕榈酸酯脂质微球注射液抗大鼠支气管哮喘的药效学

目的考察曲安奈德棕榈酸酯脂质微球注射液(triamcinolone acetonide palmitate lipid microsphere injection,TAL)对大鼠支气管哮喘的防治效果。方法用卵白蛋白(ovalbumin,OVA)致敏,激发大鼠建立哮喘动物模型,测定哮喘潜伏期、支气管内压力(pulmonary inflation pressure,PI)、支气管肺泡灌洗液(bronchoalveolar lavage fluid,BALF)中炎性细胞数,观察肺组织病理改变。结果TAL能显著延长大鼠哮喘潜伏期,降低PI值和BALF中白细胞总数和嗜酸性粒细胞(eosinophils,EOS)数;病理检查结果表明,TAL各剂量组肺部病变均有所缓解。结论TAL能够延长OVA雾化激发后大鼠的哮喘潜伏期,降低氯化乙酰胆碱激发后大鼠气管内压力,降低大鼠BLAF中白细胞总数和EOS个数,使大鼠肺部病变有所改善,对大鼠支气管哮喘有防治作用。     

小儿平喘方对哮喘大鼠血清白细胞介素-4、γ-干扰素水平的影响

目的观察小儿平喘方对哮喘模型大鼠血清中γ-干扰素(IFN-γ)、白细胞介素-4(IL-4)含量、IFN-γ/IL-4比值的影响,从而探讨小儿平喘方治疗支气管哮喘的药效机制。方法选取SD大鼠32只,随机分为4组:正常对照组、哮喘模型组、小儿平喘方小剂量组(小剂量组)和小儿平喘方大剂量组(大剂量组),每组8只,采用卵清蛋白(OVA)致敏和雾化吸入激发制备大鼠哮喘模型,用双位点夹心酶联免疫吸附试验测定各组大鼠血清中IL-4和IFN-γ含量。结果与正常对照组比较,哮喘模型组大鼠血清IFN-γ的含量与IFN-γ/IL-4比值均降低(P0.05),而IL-4的含量则显著升高(P0.05);与哮喘模型组比较,大、小剂量组大鼠血清IFN-γ的含量与IFN-γ/IL-4比值均显著升高(P0.01),而IL-4的含量则降低(P0.05)。结论小儿平喘方能显著降低支气管哮喘模型大鼠血清IL-4的含量,提高IFN-γ的含量及失衡的IFN-γ/IL-4比值,从而调节免疫功能,减轻炎症反应,控制哮喘的发作。     

滨蒿内酯对大鼠哮喘模型气道平滑肌增殖及PKC-α蛋白表达的影响

目的 观察滨蒿内酯对哮喘大鼠气道壁平滑肌增殖及PKC-α(protein kinase C-α,蛋白激酶C-α)表达的影响.探讨滨蒿内酯治疗哮喘的作用机制.方法 40只雄性人鼠随机分成4组:正常对照组(N组)、哮喘组(A组)、地塞米松治疗组(D组)及滨蒿内酯治疗组(S组),以卵清蛋白致敏和激发方法 建立哮喘人鼠动物模型并给予相应治疗.测定各组肺功能.检测支气管肺泡灌洗液(BALF)中白细胞总数及嗜酸粒细胞(EOS)计数;用免疫组化法检测PKC-α蛋白表达水平、光镜下测定平滑肌层厚度及内外径.结果 大鼠致敏2周及诱发哮喘4周后,肺功能测定表现为呼气时间延长,呼气峰压明显增大;A组BALF中的白细胞总数及Eos计数均较N组明显升高.哮喘模型组气道壁PKC-α蛋白含量和平滑肌层厚度较正常组均显著增加(均为P<0.001),气道内外径比值较正常组减小(P<0.001).气道壁平滑肌层厚度与PKC-α.蛋白表达呈正相关(rs=0.771,P<0.01).结论 滨蒿内酯能减轻哮喘大鼠气道壁平滑肌层的增厚并抑制PKC-α的表达.     

哮喘大鼠肺泡巨噬细胞电压依赖性钾通道的活性变化

目的探讨哮喘模型大鼠肺泡巨噬细胞(alveolar macrophage,AM)电压依赖性钾通道(Voltage-dependent potassiumchannel,KV)活性的变化及其对巨噬细胞功能的影响。方法利用卵蛋白(ovialbumin,OVA)致敏并激发大鼠建立哮喘模型,收集支气管肺泡灌洗液(bronchus alveolarlavagefluid,BALF)培养AM。利用全细胞电压钳模式记录AM细胞膜上的KV电流,观察比较哮喘模型组和对照组KV通道活性的变化。结果哮喘组支气管肺泡灌洗液(BALF)细胞总数显著增高,与对照组(n=7)比较差异显著(P<0.01);哮喘大鼠AM细胞KV电流幅度[(243.56±133.56)pA,n=11]较对照组[(656.23±162.34)pA,n=11]明显降低(P<0.01)。结论哮喘大鼠AM细胞KV通道活性降低,可能导致AM兴奋性增高易被激活分泌各种炎性介质和细胞因子,从而参与哮喘炎症的形成。     

红霉素对支气管哮喘大鼠Clara细胞及CC16表达的影响

目的探讨红霉素对支气管哮喘(简称哮喘)大鼠模型肺组织Clara细胞数量和Clara细胞分泌蛋白-16(CC16)表达的影响。方法用卵白蛋白(OVA)致敏、激发建立大鼠哮喘模型,随机分为正常对照组、哮喘组、红霉素组、地塞米松组。收集肺泡灌洗液(BALF)进行细胞计数及分类,光镜下观察肺组织病理学变化;ELISA方法检测BALF中CC16含量,用免疫组化的方法检测肺组织中Clara细胞表达变化。结果与正常对照组相比,哮喘组大鼠支气管及血管周围、肺间质内有嗜酸性粒细胞(EOS)及其他炎性细胞浸润,黏液腺增生,黏膜皱折增多,黏膜上皮细胞脱落,可见气道黏液栓,而红霉素组和地塞米松组上述现象明显减轻。肺组织Clara细胞计数显示,哮喘组大鼠终末及呼吸性细支气管上皮Clara细胞数明显少于正常对照组,而红霉素组和地塞米松组较哮喘组均有所增加(P<0.05)。哮喘组EOS百分比(EOS%)显著高于对照组(P<0.01),红霉素组和地塞米松组的EOS%均低于哮喘组(P<0.01)。BALF中CC16含量,哮喘组明显低于正常对照组(P<0.01),而红霉素组和地塞米松组均高于哮喘组(P<0.05)。结论哮喘时肺组织中Clara细胞及CC16的表达减少,红霉素可通过上调肺组织中Clara细胞及CC16的表达来发挥抗炎作用。     

Establishment of a rat chronic asthma model and its evaluation

This study is to establish a rat chronic asthma model. Sensitive SD rats were selected through histamine challenge. The asthmatic groups were sensitized by ih and ip with OVA, aluminium hydroxide gel and inactivated bacillus pertussis on day 1 and 14. From day 21, acute asthmatic group was aerosolized 1% OVA for 1 week, chronic asthmatic group was aerosolized 0.1% OVA for 12 weeks. The control groups received saline as the substitution of OVA. Twenty four hours after the last provocation, physiological monitoring equipment was used to detect the pulmonary function, then the rats were sacrificed. Bronchoalveolar lavage fluid (BALF) was collected to calculate the ratio of different inflammatory cells. ELISA was used to detect total IgE and OVA-specific IgE in serum. Microscopy was conducted to observe the histopathology of lung stained with haematoxylin and eosin staining. Collagen fibers were detected using Picric acid-Sirius red staining technique. The optical density at 610 nm of extractive from locus caeruleus was detected by passive cutaneous anaphylaxis (PCA). The results showed that the asthmatic characteristics were significantly developed in model groups, but not in control groups. Chronic asthmatic group had significantly higher indexes than acute asthmatic group, including the thickness of airway smooth muscle and bronchial basement membrane, and goblet cell hyperplasia, the area of collagen in airways, A610 of extractive from locus caeruleus, the concentration of total IgE and OVA-specific IgE in serum. However, inflammatory cell infiltrate in lungs and the percentage of eosinophils of white blood cells in BALF were lower in chronic asthmatic group than those in acute asthmatic group. Respiratory rate and respiratory flow showed no significant difference in both model groups. In conclusion, the rat chronic asthma model is established by the way in this study, which is comparable to the physiopathologic characteristics of human asthma.     

Oral Nigella sativa oil ameliorates ovalbumin-induced bronchial asthma in mice

Nigella sativa oil (NSO) is used in folk medicine as a therapy for many diseases including bronchial asthma. We investigated the possible modulating effects of NSO on asthma-like phenotypes in a mouse model of bronchial asthma. BALB/c mice were actively sensitized by intraperitoneal injections of 50μg ovalbumin (OVA) with 1mg alum on days 0 and 12. Starting on day 22, they were exposed to OVA (1% (w/v), in sterile physiological saline) for 30min, three times every 4th day. Negative control animals were exposed to saline in a similar manner. NSO was administered orally for 31day from day 0 to day 30. On the day of sensitization and challenge, NSO was given 30min before the treatment. Airway function, number of inflammatory cells in bronchoalveolar lavage fluid (BALF), levels of interleukin (IL)-4, IL-5, IL-13 and interferon (IFN)-γ in BALF, serum levels of total IgE, OVA-specific IgE, IgG1 and IgG2a, and histopathological examination of lung tissues were investigated. Oral treatment with NSO showed significant decrease in airway hyperresponsiveness, the number of total leukocytes, macrophages and eosinophils, levels of IL-4, IL-5 and IL-13 in BALF, serum levels of total IgE, OVA-specific IgE and IgG1, and significant increase in BALF level of IFN-γ and serum level of OVA-specific IgG2a, indicating restoration of local Th1/Th2 balance. Furthermore, it significantly abrogated the histopathological changes of the lungs, as the images were nearly normal. These results suggest that the treatment with oral NSO could be a promising treatment for bronchial asthma in humans.     

甲泼尼龙琥珀酸钠对自身免疫性肺气肿模型大鼠氧化应激和抗内皮细胞抗体的影响

目的:研究甲泼尼龙琥珀酸钠对自身免疫性肺气肿模型大鼠氧化应激和抗内皮细胞抗体(AECA)的影响。方法:将雄性SD大鼠随机分为对照组、模型组和干预组,每组8只。除对照组大鼠腹腔注射等体积的完全弗氏佐剂外,模型组和干预组大鼠均腹腔注射体外培养的人脐静脉内皮细胞+完全弗氏佐剂混合物以复制自身免疫性肺气肿模型;造模给药后第2天,干预组大鼠腹腔注射甲泼尼龙琥珀酸钠10 mg/(kg·d),对照组和模型组大鼠均腹腔注射等体积的生理盐水,每日1次,连续21 d。末次给药后,取各组大鼠右肺组织制作石蜡切片并行苏木精-伊红染色,观察肺组织病理变化,测量单位面积内的肺泡数(MAN)和内衬间隔(MLI);检测左肺肺泡灌洗液(BALF)中丙二醛(MDA)、还原型谷胱甘肽(GSH)含量和超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性,以及BALF和血清中AECA含量。采用Pearson分析模型组大鼠BALF中AECA与MDA、GSH、SOD、GSH-Px的相关性。结果:与对照组比较,模型组大鼠肺组织可见明显的肺气肿病理变化,其MAN显著减少,MLI显著延长(P<0.01);BALF中GSH含量和SOD、GSH-Px活性均显著降低,BALF中MDA含量以及BALF、血清中AECA含量均显著升高(P<0.01)。与模型组比较,干预组大鼠肺组织的肺气肿病理变化明显改善,其MAN显著增加,MLI显著缩短(P<0.01);BALF中GSH含量和SOD、GSH-Px活性均显著升高;BALF中MDA含量以及BALF、血清中AECA含量均显著降低(P<0.01)。模型组大鼠BALF中的AECA与MDA呈正相关(r=0.710,P<0.05),与GSH、SOD、GSH-Px呈负相关(r=-0.754、-0.781、-0.736,P<0.05)。结论:甲泼尼龙琥珀酸钠可能通过减轻氧化应激反应、抑制AECA的表达,从而达到预防自身免疫性肺气肿的目的。     

Propolis extracts exhibit an immunoregulatory activity in an OVA-sensitized airway inflammatory animal model

Propolis, which has been used widely in folk medicine, has been shown to exhibit various biological activities but its immunoregulatory and anti-inflammatory activities in intact animals have not been well studied. We investigated these activities of propolis using an ovalbumin-induced asthma animal model. Mice were immunized and sensitized by exposure to ovalbumin (OVA) antigen and administered with low- (65 mg/kg body weight) and high-dose (325 mg/kg body weight) propolis water extracts by tube feeding. The serum OVA-specific IgE titer and cytokine profiles in cultured splenocytes and bronchoalveolar lavage fluids (BALF) were analyzed. The number of eosinophils in BALF was counted. Here we demonstrate that propolis extracts can suppress the serum levels of OVA-specific IgE and IgG(1), and airway hyperresponsiveness (AHR) in OVA-sensitized mice. There are no significant differences in the concentration of eotaxin or the number of eosinophils in BALF among the four groups. However, the higher dose of propolis extracts decreases the level of IL-5 in BALF. The splenocytes from mice administered with propolis extracts (low- and high-dose groups) exhibit a strong inhibition of IL-10 secretion and up-regulation of IFN-gamma secretion in splenocytes stimulated with concanavalin A (ConA). In addition, cytokine (IFN-gamma, IL-6, and IL-10) secretion in OVA-stimulated splenocytes from the propolis groups was significantly lower than that in the control group. These results suggest that propolis extracts may be a potential novel therapeutic agent for asthma.     

胆红素对实验性肺气肿支气管上皮细胞的影响

目的 :研究胆红素对吸烟所致肺气肿大鼠支气管上皮细胞的影响。方法 :应用被动吸烟的方法复制大鼠肺气肿模型 ,采用透射电镜和光镜观察大鼠支气管上皮细胞的病理变化 ,用免疫组织化学方法检测支气管上皮细胞间黏附分子 1(ICAM 1)蛋白表达的变化 ,用放射免疫分析法检测支气管肺泡灌洗液肿瘤坏死因子α(TNF α)浓度。结果 :模型组支气管黏膜上皮细胞缺失 ,杯状细胞大量增生 ,上皮细胞纤毛脱落、排列紊乱 ,线粒体肿胀 ,嵴断裂、消失 ,内质网扩张 ,肺泡腔内可见坏死脱落的上皮及渗出物。对照组支气管上皮细胞完整 ,纤毛排列整齐 ,细胞内线粒体、内质网形态正常。胆红素干预组黏膜上皮细胞基本完整 ,上皮细胞纤毛轻度脱落 ,线粒体、内质网改变较轻。支气管肺泡灌洗液中TNF α浓度 ,模型组及胆红素干预组均高于对照组 (P <0 .0 1) ,与模型组比较 ,胆红素干预组TNF α浓度均明显降低 (P <0 .0 5 )。模型组及胆红素干预组支气管上皮细胞ICAM 1表达高于对照组 (P <0 .0 1) ,胆红素干预组ICAM 1表达水平低于模型组 (P <0 .0 5 )。相关分析结果显示 :模型组支气管肺泡灌洗液中 ,TNF α浓度与支气管上皮细胞的ICAM 1表达呈正相关 (r=0 .72 ,P <0 .0 5 )。结论 :由吸烟所致的大鼠肺气肿支气管上皮细胞表达ICAM 1升高     

咳喘宁粉剂治疗支气管哮喘的临床与实验研究

目的：探讨咳喘宁粉剂治疗支气管哮喘的疗效及部分作用机理。方法：观察支气管哮喘患儿服用咳喘宁粉剂前后的肺功能，血清IgE水平以及给药1年后的临床控制率；动物实验观察正常对照组、哮喘组、咳喘宁组的引喘潜伏期，肺泡灌洗液(BALF)，一氧化氮(NO)和内皮素—1(ET-1)水平。结果：咳喘宁粉剂不仅可以改善哮喘患儿肺功能，使异常升高的IgE下降，显示较好的临床控制率，而且显延长豚鼠引喘潜伏期、降低BALF的NO和ET-1水平。结论：咳喘宁粉剂对儿童支气管哮喘有较好治疗作用，此作用可能与其减少IgE、NO和ET-1生成有关。     

左西替利嗪治疗支气管哮喘的疗效及可能机制

目的:研究左西替利嗪治疗哮喘的疗效及可能的机制。方法:以卵蛋白致敏法制备大鼠哮喘模型,40只SD大鼠随机分为5组,即正常对照组、哮喘组、地塞米松组、左西替利嗪高剂量组、左西替利嗪低剂量组,各组连续治疗与激发7d后取材。采用ELISA法测定大鼠血清中白细胞介素4(IL-4)、白细胞介素5(IL-5)、肿瘤坏死因子α(TNF-α)的含量;进行支气管肺泡灌洗液(BALF)细胞计数、肺组织嗜酸粒细胞(Eos)计数及病理学观察等。结果:哮喘组IL-4、IL-5、TNF-α较正常对照组均有显著增加(P<0.01);地塞米松组IL-5、TNF-α水平较哮喘组显著降低(P<0.01);左西替利嗪高、低剂量组IL-4、IL-5、TNF-α均较哮喘组减少(P<0.05或P<0.01)。哮喘组BALF中白细胞总数和肺组织Eos计数较正常对照组明显增加(P<0.01);地塞米松组较哮喘组显著减少(P<0.01);左西替利嗪高、低剂量组BALF中白细胞总数与哮喘组相比明显减少(P<0.01),而其肺组织Eos计数与哮喘组相比无显著差异,明显高于地塞米松组(P<0.01)。病理组织学检查可见哮喘组支气管及血管周围有大量Eos浸润等改变,地塞米松组及左西替利嗪高、低剂量组肺组织病理改变均不同程度的轻于哮喘组。结论:左西替利嗪能显著降低哮喘相关细胞因子的水平,因此其可能成为一种新的治疗哮喘的药物。     

槐杞黄对哮喘大鼠BALF中IL-5及INF-γ的影响

目的观察槐杞黄对大鼠哮喘模型BALF中IL-5及INF-γ的影响。方法大鼠40只,随机分成4组:正常对照组(N组)、哮喘模型组(A组)、地塞米松组(D组)、地塞米松+槐杞黄组(H组),复制哮喘模型。用细胞计数板计算支气管肺泡灌洗(BALF)中细胞总数和嗜酸性粒细胞(EOS)数;酶联免疫吸附法(ELISA)检测血清卵蛋白特异性IgE(OVA-IgE)和BALF中白介素-5(IL-5)、INF-γ的水平。结果 A组血清OVA-IgE、BALF中EOS数和IL-5水平高于N组(P<0.05);D组和H组各指标较A组下降(P<0.05);H组各指标较D组下降(P<0.05),与N组比较,差异无统计学意义(P>0.05)。A组BALF中INF-γ的水平低于N组,两组比较,差异有统计学意义(P<0.05);D组和H组各指标较A组回升(P<0.05);H组较D组进一步回升(P<0.05),与N组比较,差异无统计学意义(P>0.05)。结论槐杞黄辅助治疗可以抑制哮喘大鼠OVA-IgE和IL-5合成,促进INF-γ合成,调节Th1/Th2平衡,从而发挥其抗EOS性气道炎症的作用。     

哮喘患者血清中IL-4、IL-18和IgE水平的变化和意义

目的探讨血清中IL-4、IL-18和IgE水平变化在哮喘患者中的意义。方法选取2009年12月至2010年12月来我院呼吸内科诊治的支气管哮喘患者30例及同期在院体检的健康者20例为对照,采用酶联免疫吸附实验法(ELISA)检测患者及对照组血清中IL-4、IL-18和IgE水平。结果 IL-4、IL-18和IgE水平在哮喘患者比对照组明显升高,差异有统计学意义(P<0.05)。并且在哮喘患者中,急性发作组三者的水平较缓解组也升高,差异有统计学意义(P<0.05)。结论血清中IL-4、IL-18和IgE水平增加与支气管哮喘发病密切相关。     

培土生金法对脾虚哮喘模型大鼠NF-κB表达的影响

目的观察培土生金法对脾虚哮喘模型大鼠TNF-α/NF-κB信号通路变化的影响,探讨培土生金法干预哮喘气道炎症和黏液高分泌的信号转导机制。方法健康雄性Wistar大鼠50只,随机分成5组:对照组、脾虚哮喘组、哮喘组、脾虚哮喘治疗组和哮喘治疗组,每组10只。采用ELISA试剂盒法测定血清和BALF中TNF-α的含量,采用免疫组化测定大鼠肺组织NF-κBp65的表达和入核率。结果脾虚哮喘组和哮喘组血清和BALF中TNF-α含量及大鼠支气管上皮细胞中NF-κBp65阳性表达均显著升高,和对照组比较差异显著(P<0.01);但是脾虚哮喘组和哮喘组比较,血清和BALF中TNF-α含量无显著性差异。与哮喘组比较,脾虚哮喘组大鼠支气管上皮细胞中NF-κBp65入核率显著增加(P<0.01)。和脾虚哮喘组比较,脾虚哮喘治疗组血清和BALF中TNF-α含量及肺组织NF-κBp65入核率显著降低(P<0.01);和哮喘组比较,哮喘治疗组血清和BALF中TNF-α含量及肺组织NF-κBp65入核率显著降低(P<0.01)。结论培土生金法能够降低脾虚哮喘和哮喘大鼠血清和BALF中TNF-α的含量和肺组织NF-κBp65入核率。