三氧化二砷对哮喘小鼠肺内树突状细胞的影响

目的 :研究不同浓度三氧化二砷 (arsenictrioxide ,As2 O3)对哮喘小鼠肺内树突状细胞 (dendriticcell,DC)分布、募集的影响及其作用机制。方法 :BALB/c小鼠 5 0只随机分为 5组 ,即对照组、哮喘组、低剂量 (1mg/kg)As2 O3组、中剂量 (5mg/kg)As2 O3组和高剂量 (10mg/kg)As2 O3组。采用免疫组织化学染色技术检测小鼠肺、气道DC ;计算机图像分析技术对DC进行定量测定 ;扫描电镜分析DC形态。结果 :对照组小鼠整个肺组织包括气管、支气管、肺泡和脏层胸膜构成了一个NLDC -14 5 +DC网络 ,NLDC -14 5 + DC密度从大气道到小气道分别为 (5 0 0± 5 0 )个 /mm2 到 (60± 10 )个 /mm2 上皮面积 (P <0 0 5 ) ,扫描电镜下DC呈典型的树突状形态 ;哮喘组小鼠肺内NLDC -14 5 + DC密度较对照组显著增加 (P <0 0 1) ;哮喘小鼠经As2 O3处理后 ,肺内DC密度皆显著下降 (P <0 0 1) ,但三种不同浓度砷剂处理组间无显著性差异 (P >0 0 5 )。结论 :下调肺内DC数量可能是As2 O3治疗哮喘的一个重要机制 ;低剂量As2 O3治疗哮喘既安全又有效 ,具有潜在的应用前景。     

微波消融联合树突状细胞瘤苗免疫治疗小鼠乳腺癌的疗效及免疫学机制探讨

目的观察微波消融联合树突状细胞（DC）瘤苗免疫治疗小鼠乳腺癌的疗效并探讨其免疫学机制。 方法采用随机数字表法将48只BALB/c小鼠分为模型组、微波消融组、DC瘤苗免疫组及联合治疗组。将上述小鼠制成乳腺癌实验动物模型，微波消融组于荷瘤14d时给予微波消融治疗，DC瘤苗免疫组于荷瘤7d时给予DC瘤苗免疫，联合治疗组分别于上述时间点给予DC瘤苗免疫及微波消融治疗。观察各组小鼠存活、肿瘤生长及肺转移情况；于微波消融处理完后第14天时采用流式细胞术检测各组小鼠脾细胞中CD3+、CD4+  T细胞比例变化；采用酶联免疫吸附法（ELISA法）检测各组小鼠血清干扰素-γ（IFN-γ）和白介素-4（IL-4）水平。 结果联合治疗组小鼠存活时间［(56.4±4.3)d］、肿瘤面积［(67.3±6.1)mm2］及肺转移指数(0.6±0.4)均明显优于微波消融组及DC瘤苗免疫组（P<0.05）；联合治疗组脾细胞中CD3+ T细胞比例［(27.8±10.3)%］、CD4+ T细胞比例［(16.7±8.3)%］均较微波消融组及DC瘤苗免疫组明显增加（P<0.05）；另外联合治疗组血清中IFN-γ浓度［(41.8±22.9)pg/ml］较微波消融组及DC瘤苗免疫组显著升高（P<0.05），而IL-4浓度［(15.4±6.4)pg/ml］则较微波消融组及DC瘤苗免疫组明显降低（P<0.05）。 结论联合采用微波消融及DC瘤苗免疫治疗乳腺癌小鼠具有协同作用，与单纯微波消融或DC瘤苗免疫比较，该联合疗法能进一步抑制实验小鼠乳腺癌肿瘤生长，其治疗机制可能与增强小鼠免疫反应有关。     

重度哮喘小鼠模型的建立

目的评价用呼吸道合胞病毒(RSV)诱导致敏小鼠建立重度哮喘模型的方法。方法采用随机数字表法将30只Balb/C小鼠分为3组:磷酸盐缓冲液(PBS)对照组、卵白蛋白(OVA)组和OVA/RSV组。采用OVA腹腔注射致敏、结合OVA持续雾化吸入及RSV(1.0×109pfu/L,50μl)多次滴鼻激发的方法复制重度哮喘动物模型。观察小鼠哮喘发作症状;用动物体描箱法测定肺功能变化,包括用力最大呼气流速(PEF)、第0.4秒用力呼气容积/用力肺活量(FEV0.4/FVC)及乙酰胆碱(Ach)激发条件下气道反应性以肺阻力(RL)表示;苏木素-伊红(HE)、过碘酸-希夫(PAS)、Masson染色观察动物肺组织大体变化、炎性细胞浸润、杯状细胞增生、黏液分泌及气道重塑变化,同时测定气道壁内径/外径比值及气道平滑肌层、网状基底膜层厚度。结果1以5.0、15.0和45.0g/LAch激发时,OVA组和OVA/RSV组RL、PEF和FEV0.4/FVC均较对照组差异有显著性(P均<0.01);与OVA组比较,OVA/RSV组小鼠喘息症状加重,RL明显升高,而PEF和FEV0.4/FVC则均明显下降(P均<0.01);气道黏膜下淋巴细胞、嗜酸粒细胞、中性粒细胞浸润明显加重,气道黏膜上皮增生、黏液分泌及气道周围胶原沉积增加。2OVA/RSV组气道壁内径/外径比值、气道平滑肌层和网状基底膜层厚度分别为0.56±0.03、(45.12±2.08)μm和(36.15±1.88)μm,OVA组分别为0.75±0.06、(24.63±0.94)μm和(21.68±1.13)μm,两组间及两组与对照组比较差异均有显著性(P均<0.01)。结论用RSV诱导致敏小鼠建立重度哮喘模型是有效的方法。     

调节性T细胞表达CD39和CD73在小鼠哮喘模型发病中的作用

目的:探讨CD39和CD73阳性的CD4+CD25+Foxp3+T淋巴细胞(Treg细胞)对支气管哮喘(简称哮喘)小鼠气道炎症的影响。方法:将16只BALB/c成年雌性小鼠随机分为哮喘组(n=8)和对照组(n=8)。用卵清蛋白进行哮喘造模后,取小鼠血清检测总Ig E,采用高效液相色谱法行支气管肺泡灌洗液上清液三磷酸腺苷(adenosine-triphosphate,ATP)检测,取左肺组织行苏木精-伊红(hematoxylin eosin,HE)染色,观察小鼠肺组织的炎症改变;右肺上叶行CD39 m RNA、CD73 m RNA、Foxp3 m RNA检测;余右肺制成单细胞悬液,采用流式细胞术检测CD39+Treg和CD73+Treg细胞数量,计算其占Treg细胞百分比。结果 :哮喘组小鼠的血清总Ig E较对照组显著上升(P<0.01),支气管肺泡灌洗液中ATP较对照组升高(P<0.05)。流式细胞术检测发现,哮喘组小鼠肺组织的CD39+Treg、CD73+Treg细胞百分比较对照组略有下降趋势,但差异尚无统计学意义。结论:肺局部CD39+Treg和CD73+Treg细胞数量减少和(或)功能障碍导致的细胞外ATP清除率降低,可能是哮喘气道炎症发生的重要机制之一。     

哮喘豚鼠支气管肺组织IL-5及GM-CSFmRNA表达

目的 :探讨白介素 5 (IL 5 )及粒细胞 巨噬细胞集落刺激因子 (GM CSF)在哮喘豚鼠支气管肺组织中的表达。方法 :实验分为哮喘组和对照组 ,每组各 15只豚鼠。采用原位杂交方法检测两组豚鼠支气管肺组织的IL 5和GM CSFmRNA表达。结果 :哮喘组支气管肺组织IL 5和GM CSFmRNA表达强度 (细胞数 /HP)分别为 36 0 0± 8 0 0和 32 0 0± 9 0 0 ,对照组分别为 14 0 0± 5 0 0和 18 0 0± 7 0 0 ,哮喘组IL 5和GM CSFmRNA表达强度显著高于对照组 (P <0 0 1)。哮喘组肺组织嗜酸细胞 (EOS)浸润密度 (细胞数 /HP)为 48 0 0± 2 6 0 0 ,对照组为 19 0 0± 6 0 0 ,哮喘组显著高于对照组 (P <0 0 1)。结论 :哮喘豚鼠支气管肺组织IL 5和GM CSFmRNA高表达可能在气道炎症中发挥重要作用。     

树突状细胞在多发伤中的变化及临床意义

目的探讨多发伤树突状细胞(DC)变化及临床意义。方法从68例多发伤患者和22例健康人外周血中分别提取DC;通过流式细胞仪分别检测各组的DC数量,DC表面HLA-DR、CD80、CD86表达水平以及DC诱导的T细胞反应性增殖情况。同时检测各组中IL-6I、L-10的浓度。结果多发伤组DC细胞数〔(8.3±2.8)×106/L〕明显低于对照组〔(15.2±4.1)×106/L,P<0.01〕。多发伤组DC表面HLA-DR及CD80、CD86的表达水平与对照组相比明显降低(P<0.01)。DC诱导的T细胞增殖能力对照组明显强于创伤组(P<0.01)。多发伤组血清IL-6、IL-10的浓度显著升高,与对照组比较差异有非常显著性意义(P<0.01)。结论多发伤患者DC数量明显减少且功能下降,这可能与创伤后的免疫功能低下密切相关。     

大鼠脑缺血后胶质细胞向树突状细胞转化的研究

目的探讨树突状细胞( dendritic cells,DC)是否参与脑缺血损伤过程及在缺血脑组织中 DC的来源. 方法用线栓方法封闭大鼠右侧大脑中动脉制作动物模型.用免疫组化方法检测脑缺血 1 h到第 6 天时,缺血脑 DC( OX62+)的存在,以及胶质细胞 /巨噬细胞( OX42+)转化成 DC( OX62+),同时检测活化后的 DC样细胞表达主要组织相容性复合分子Ⅱ( MHCⅡ)情况. 结果脑缺血半球和假手术半球比较,在 1 h DC数量增加 (t=7.143, P< 0.001),在脑缺血组中,缺血脑半球与非缺血脑半球比, DC的数量也增多 (t=4.968, P< 0.01).脑缺血第 6天缺血组与假手术组进行比较, DC表达 MHCⅡ( OX62+ OX6+)显著差异,每 100 mm2脑组织切片中 OX62+ OX6+细胞数量比为 (53± 3)比 (33± 2)个 (t=2.975, P< 0.05).脑缺血半球在 1 h到第 6天 OX42+转变成 OX62+ OX42+细胞逐渐增加,脑缺血第 6天脑缺血半球与非缺血半球比 t=9.875, P< 0.001.脑缺血损伤面积与以每 100 mm2脑组织片为单位的 OX62+数量呈正相关 (R2=0.891 4,P< 0.001). 结论脑缺血后,脑缺血组织中 DC的数量增加, DC数量增加与脑伤面积呈正相关,提示 DC参与了脑缺血过程,大鼠脑缺血后从胶质细胞向 DC样细胞转化是脑内 DC的来源之一.     

环磷酰胺联合树突状细胞分泌的外泌体和PolyⅠ:C的抗肿瘤作用研究

目的观察树突状细胞(DC)分泌的外泌体(exosomes)与环磷酰胺(CTX)、PolyⅠ∶C联合应用的抗肿瘤效果。方法重组鼠粒细胞-单核细胞集落刺激因子诱导骨髓来源的造血干细胞分化为髓系树突状细胞,肿瘤细胞L1210的冻融抗原负载树突状细胞,以超速离心结合膜过滤的方法提取外泌体;用得到的外泌体在DC存在的情况下刺激T细胞,应用cck-8试剂盒测量T细胞的增殖;制备抗原特异性的细胞毒性T淋巴细胞(CTL),通过DIOC-18联PI的方法测定CTL对肿瘤的杀伤作用;L1210细胞接种小鼠,制备荷瘤小鼠模型,分为实验组(exosomes联合CTX和PolyⅠ∶C)和对照组(1.PBS组,2.CTX组,3.CTX+PolyⅠ∶C组4.exosomes组)作治疗,观察肿瘤的生长速度,小鼠的生存期。结果T细胞的增殖实验中,平均吸光度:实验组为0.90±0.22,对照组为0.53±0.13,差异具有统计学意义(P<0.05)。负载肿瘤抗原的exosomes刺激的CTL在体外能够特异性杀伤肿瘤细胞L1210,在效靶比分别为5∶1和10∶1时实验组的杀伤率分别为(21.19±3.99)%、(30.56±3.85)%,对照组的杀伤率分别为(17.54±4.48)%、(19.38±4.68)%,10∶1时实验组与对照组相比杀伤率差异具有统计学意义(P<0.05);与对照组相比,实验组荷瘤小鼠的肿瘤生长速度明显降低,小鼠的生存期延长。结论经过肿瘤抗原负载的exosomes刺激的T细胞体外能够杀伤肿瘤细胞;exosomes联合CTX和PolyⅠ∶C能显著抑制荷瘤小鼠体内肿瘤的生长,延长荷瘤小鼠的生存期。     

反义GATA-3治疗哮喘气道炎症的实验研究

目的:观察反义GATA-3治疗大鼠哮喘模型气道炎症的作用。方法:按常用方法制作大鼠哮喘模型并分为哮喘组(A组),地塞米松治疗组(D组),GATA-3反义寡核苷酸治疗组(AS组),GATA-3无意义寡核苷酸治疗组(NS组)和正常对照组(N组)5组,每组10只。反义寡核苷酸和无意义寡核苷酸经鼻气管内给药,地塞米松腹腔注射给药。用HE染色的方法观察气道炎症变化。免疫组化方法观察GATA-3阳性细胞数。用RT-PCR方法观察大鼠肺组织GATA-3mRNA表达。用Western蛋白印迹法检测肺组织中GATA-3蛋白质表达。结果:与N组相比,A组GATA-3mRNA和蛋白质的表达量及气道炎性细胞浸润数量明显增加(P<0.01)。AS组和D组GATA-3mRNA和蛋白质表达量及气道炎性细胞浸润数量与A组相比均明显降低(P<0.01)。NS组GATA-3mRNA和蛋白质表达量和炎性细胞浸润数量与A组相比差异无显著性(P>0.05)。GATA-3的表达与大鼠支气管肺组织中嗜酸性粒细胞浸润数量呈正相关,相关系数为0.995(P<0.01)。结论:GATA-3反义寡核苷酸能特异性地抑制GATA-3基因的表达,减轻气道炎症反应。GA...     

流式细胞仪测检外周血树突状细胞及临床应用

目的建立简便可靠的外周血树突状细胞DC1、DC2亚群检测方法,探讨DC1、DC2亚群在慢性乙型肝炎患者中改变的意义。方法用流式细胞仪检测27名健康人、29例慢性乙型肝炎患者及19例肝炎肝硬化患者外周血树突状细胞亚群。DC1不表达lin(CD19、CD20、CD56、CD14、CD3),但高表达HLA-DR及CD11c;DC2不表达lin(CD19、CD20、CD56、CD14、CD3),高表达HLA-DR及CD123。结果健康人组外周血DC1为(0.28±0.07)%,绝对计数为(18.6±5.3)×106/L,DC2为(0.22±0.09)%,绝对计数为(14.4±5.8)×106/L。慢性肝炎组DC1变化不明显(P>0.05),DC2百分比和绝对数显著下降(P<0.005),DC1/DC2升高(P<0.005)。肝炎肝硬化患者组DC1、DC2与对照组比较均明显减少(P<0.005)。结论流式细胞仪检测外周血树突状细胞亚群简便、可靠,适合于临床常规开展。DC1、DC2检测在慢性乙型肝炎和肝硬化患者的疾病进程及机体免疫状况评价方面具有重要的临床价值。     

Enhanced reactive lysis of paroxysmal nocturnal hemoglobinuria erythrocytes. Studies on C9 binding and incorporation into high molecular weight complexes

An mAb, NLDC-145, is described that specifically reacts with a group of nonlymphoid dendritic cells including Langerhans cells (LC), veiled cells (VC), and interdigitating cells (IDC). The antibody does not react with precursor cells in bone marrow and blood. Macrophages are not stained by the antibody, but a subpopulation of Ia+ peritoneal exudate cells is recognized. Possible relationships of the various nonlymphoid dendritic cell (NLDC) types are discussed.     

Characterization of murine lung dendritic cells: similarities to Langerhans cells and thymic dendritic cells

Dendritic cells (DC) are potent accessory cells (AC) for the initiation of primary immune responses. Although murine lymphoid DC and Langerhans cells have been extensively characterized, DC from murine lung have been incompletely described. We isolated cells from enzyme-digested murine lungs and bronchoalveolar lavages that were potent stimulators of a primary mixed lymphocyte response (MLR). The AC had a low buoyant density, were loosely adherent and nonphagocytic. AC function was unaffected by depletion of cells expressing the splenic DC marker, 33D1. In addition, antibody and complement depletion of cells bearing the macrophage marker F4/80, or removal of phagocytic cells with silica also failed to decrease AC activity. In contrast, AC function was decreased by depletion of cells expressing the markers J11d and the low affinity interleukin 2 receptor (IL-2R), both present on thymic and skin DC. AC function was approximately equal in FcR+ and FcR- subpopulations, indicating there was heterogeneity within the AC population. Consistent with the functional data, a combined two-color immunofluorescence and latex bead uptake technique revealed that lung cells high in AC activity were enriched in brightly Ia+ dendritic-shaped cells that (a) were nonphagocytic, (b) lacked specific T and B lymphocyte markers and the macrophage marker F4/80, but (c) frequently expressed C3biR, low affinity IL-2R, FcRII, and the markers NLDC-145 and J11d. Taken together, the functional and phenotypic data suggest the lung cells that stimulate resting T cells in an MLR and that might be important in local pulmonary immune responses are DC that bear functional and phenotypic similarity to other tissues DC, such as Langerhans cells and thymic DC.     

Dendritic cells pulsed with RNA are potent antigen-presenting cells in vitro and in vivo

Immunization with defined tumor antigens is currently limited to a small number of cancers where candidates for tumor rejection antigens have been identified. In this study we investigated whether pulsing dendritic cells (DC) with tumor-derived RNA is an effective way to induce CTL and tumor immunity. DC pulsed with in vitro synthesized chicken ovalbumin (OVA) RNA were more effective than OVA peptide-pulsed DC in stimulating primary, OVA-specific CTL responses in vitro. DC pulsed with unfractionated RNA (total or polyA+) from OVA-expressing tumor cells were as effective as DC pulsed with OVA peptide at stimulating CTL responses. Induction of OVA-specific CTL was abrogated when polyA+ RNA from OVA-expressing cells was treated with an OVA- specific antisense oligodeoxynucleotide and RNase H, showing that sensitization of DC was indeed mediated by OVA RNA. Mice vaccinated with DC pulsed with RNA from OVA-expressing tumor cells were protected against a challenge with OVA-expressing tumor cells. In the poorly immunogenic, highly metastatic, B16/F10.9 tumor model a dramatic reduction in lung metastases was observed in mice vaccinated with DC pulsed with tumor-derived RNA (total or polyA+, but not polyA- RNA). The finding that RNA transcribed in vitro from cDNA cloned in a bacterial plasmid was highly effective in sensitizing DC shows that amplification of the antigenic content from a small number of tumor cells is feasible, thus expanding the potential use of RNA-pulsed DC- based vaccines for patients bearing very small, possibly microscopic, tumors.     

雾化吸入BCG对哮喘小鼠气道炎性作用的影响

目的探讨卡介苗（BCG）雾化吸入对变应性哮喘的治疗作用及其与支气管肺泡灌洗液（BALF）中γ-干扰素（IFN-γ）的关系。方法昆明小鼠32只，随机分成三组，正常对照组，哮喘模型组及治疗组。治疗组又分为BCG治疗组和地塞米松治疗组。治疗组与哮喘模型组一起制作哮喘模型。观察小鼠气道壁炎症变化，并收集支气管肺泡灌洗液（BALF），测定BALF中细胞总数，嗜酸性粒细胞和淋巴细胞数，用酶联免疫法测定BALF中IFN-γ的含量。结果哮喘模型组BALF中细胞总数和嗜酸细胞数显著高于正常对照组（P〈0．01），BALF中IFN-γ水平显著低于正常组（P〈0．01）；BCG治疗组、地塞米松治疗组BALF中细胞数、EOS细胞数显著低于哮喘组，而IFN-γ水平显著高于哮喘组（P〈0．01）。BCG治疗组各项指标与地塞米松治疗组相比差异无统计学意义（P〉0．05）。结论雾化吸入BCG能明显抑制哮喘小鼠气道的炎性反应，吸入BCG对哮喘小鼠有治疗作用。     

糖皮质激素对哮喘小鼠CD4^＋CD25^＋调节性T细胞和TLR4表达的影响

目的探讨糖皮质激素对哮喘小鼠CD4＋CD25＋调节性T细胞（regulatory T cells,Tr）及Toll样受体4（TLR4）表达的影响。方法将雌性BALB/c小鼠30只按随机数字表法分成正常对照组（NS）、哮喘组（OVA）和哮喘糖皮质激素治疗组（OVA/GC）制备动物模型,每组10只。取小鼠左肺组织作病理切片观察炎症改变;同时应用流式细胞检测技术检测各组小鼠脾单个核细胞CD4＋CD25＋Tr占CD4＋T细胞的百分率及CD4＋CD25＋Tr上的TLR4平均荧光强度。结果哮喘小鼠脾单个核细胞CD4＋CD25＋Tr百分率明显降低（P〈0.01）,但该细胞上表达的TLR4平均荧光强度值与正常对照组差异无统计学意义（P〉0.05）;经糖皮质激素治疗后哮喘小鼠CD4＋CD25＋Tr百分率和该细胞上表达的TLR4平均荧光强度均明显升高,差异有统计学意义（P〈0.01）。结论糖皮质激素可促进哮喘小鼠CD4＋CD25＋Tr数量的增加及TLR4的表达,可能是治疗哮喘的免疫学机制之一。     

Interleukin-8 receptor modulates IgE production and B-cell expansion and trafficking in allergen-induced pulmonary inflammation

We examined the role of the interleukin-8 (IL-8) receptor in a murine model of allergen-induced pulmonary inflammation using mice with a targeted deletion of the murine IL-8 receptor homologue (IL-8r-/-). Wild-type (Wt) and IL-8r-/- mice were systemically immunized to ovalbumin (OVA) and were exposed with either single or multiple challenge of aerosolized phosphate-buffered saline (OVA/PBS) or OVA (OVA/OVA). Analysis of cells recovered from bronchoalveolar lavage (BAL) revealed a diminished recruitment of neutrophils to the airway lumen after single challenge in IL-8r-/- mice compared with Wt mice, whereas multiply challenged IL-8r-/- mice had increased B cells and fewer neutrophils compared with Wt mice. Both Wt and IL-8r-/- OVA/OVA mice recruited similar numbers of eosinophils to the BAL fluid and exhibited comparable degrees of pulmonary inflammation histologically. Both total and OVA-specific IgE levels were greater in multiply challenged IL-8r-/- OVA/OVA mice than in Wt mice. Both the IL-8r-/- OVA/OVA and OVA/PBS mice were significantly less responsive to methacholine than their respective Wt groups, but both Wt and IL-8r mice showed similar degrees of enhancement after multiple allergen challenge. The data demonstrate that the IL-8r modulates IgE production, airway responsiveness, and the composition of the cells (B cells and neutrophils) recruited to the airway lumen in response to antigen.     

哮喘小鼠肺组织STAT5、STAT6表达及阿奇霉素的影响

目的观察阿奇霉素(AZM)对哮喘小鼠信号转导和转录激活因子5、6(STAT5、STAT6)的影响。方法 BALB/c小鼠24只随机分为三组,A组(哮喘模型组)、B组(阿奇霉素治疗组)、C组(正常对照组)。其中A、B组小鼠于第0、13天分别给予卵清蛋白(OVA)20μg和氢氧化铝1 mg的混悬液致敏,于第21-30天每天给予雾化吸入2%OVA建立哮喘模型,B组于15-30天给予阿奇霉素100 mg/kg/d腹腔注射,C组以0.9%生理盐水代替OVA致敏和激发。所有动物于31天处死,制备肺组织石蜡切片,应用免疫组化方法检测支气管肺组织STAT5、STAT6的表达水平。结果哮喘模型组STAT5、STAT6蛋白表达分别为(23.25±3.28)和(26.11±3.95)明显高于正常对照组(2.33±0.78)和(2.78±0.32)(P0.01),阿奇霉素治疗组STAT5、STAT6蛋白表达分别为(10.83±1.96)和(11.32±2.03)明显低于哮喘组(P0.01)。结论 STAT5S、TAT6与哮喘发病相关,阿奇霉素可通过下调STAT5、STAT6的表达抑制气道炎症。     

黄芩苷与甘草甜素合用对豚鼠实验性哮喘的影响

目的观察黄芩苷与甘草甜素合用对豚鼠实验性哮喘的影响，并初步探讨其机制。方法健康豚鼠30只，随机分为5组，即：正常对照组，哮喘模型组，黄芩苷组，甘草甜素组及黄苷合用组，每组6只。以卵白蛋白（0vA）腹腔注射致敏和雾化吸入激发建立哮喘豚鼠模型。观察豚鼠引喘潜伏期，并检测血清NO、T—NOS、iNOS水平。结果黄芩苷与甘草甜素合用能明显延长引喘潜伏期，降低血清NO及iNOS水平，与模型组比较差异显著（P〈0．05）。结论黄芩苷与甘草甜素合用对豚鼠哮喘具有明显改善作用，可能与两者合用后抑制NO合成的作用增强有关。