从“肺与大肠相表里”探究鼠李糖乳杆菌对过敏性哮喘小鼠ERK1/2和p38 MAPK通路的影响

目的 基于“肺与大肠相表里”理论探讨鼠李糖乳杆菌对过敏性哮喘小鼠细胞外信号调节蛋白激酶1/2(ERK1/2)和p38丝裂原激活蛋白激酶(p38 MAPK)通路及相关免疫细胞的影响。方法 将18只雌性C57BL/6小鼠随机分为对照组、模型组、鼠李糖乳杆菌组，每组6只。采用卵白蛋白(OVA)致敏加激发方法构建小鼠过敏性哮喘模型，鼠李糖乳杆菌组于雾化激发前给予鼠李糖乳杆菌灌胃，连续7 d,对照组和模型组给予等量生理盐水灌胃。末次灌胃后取各组小鼠肺组织和结肠组织，HE染色进行组织病理观察；ELISA法检测血清OVA特异性IgE含量，流式细胞术检测肺组织中2型固有淋巴样细胞(ILC2)比例，Western blot法检测肺组织中p-ERK1/2和p-p38 MAPK表达情况。结果 与对照组比较，模型组小鼠支气管及血管周围存在明显炎症细胞浸润，部分肺泡结构消失；结肠腺体排列紊乱，隐窝和杯状细胞明显减少，黏膜及黏膜下层炎性细胞浸润；血清OVA特异性IgE含量、肺组织中ILC2比例、肺组织中p-ERK1/2及p-p38 MAPK相对表达量均明显升高(P均<0.05)。与模型组比较，鼠李糖乳杆菌组...     

柴朴汤对哮喘模型大鼠气道炎症及ERK/p38 MAPK信号通路的影响

目的:观察柴朴汤对哮喘模型大鼠气道炎症及细胞外信号调节激酶(ERK)/p38丝裂原活化蛋白激酶(p38MAPK)信号通路的影响。方法:SD大鼠随机分为空白组、模型组、柴朴汤低、中、高(0.75,1.5,3.0 g·kg-1)组,地塞米松组。采用卵蛋白(OVA)致敏激发建立大鼠哮喘模型。柴朴汤低、中、高剂量组于激发前0.5 h给予相应剂量柴朴汤灌胃;地塞米松组于激发前0.5 h给予地塞米松(0.005 g·kg-1)灌胃;模型组于激发前0.5 h给予等体积生理盐水灌胃;空白组以生理盐水代替OVA进行腹腔注射及雾化吸入;隔日1次,共激发28 d。观察各组大鼠支气管肺泡灌洗液(BALF)中细胞总数及分类细胞计数的变化;酶联免疫吸附法(ELISA)检测肺组织磷酸化ERK(p-ERK),磷酸化p38 MAPK(p-p38 MAPK)的活性;实时荧光定量PCR(Real-time PCR)分析检测ERK,p38 MAPK mRNA的表达;蛋白免疫印迹法(Western blot)检测ERK,p-ERK,p38MAPK,p-p38 MAPK蛋白的表达;光镜下观察病理组织形态学变化及进行炎症评分。结果:模型组大鼠BALF中细胞总数和分类细胞计数;肺组织p-ERK,p-p38 MAPK的活性,ERK,p38 MAPK mRNA的表达,p-ERK,p-p38 MAPK的表达,炎症评分均明显高于空白组(P0.01);柴朴汤低、中、高剂量组和地塞米松组上述指标则明显低于模型组(P0.05,P0.01)。结论:柴朴汤可改善哮喘模型大鼠气道炎症,其机制可能与其抑制ERK/p38 MAPK信号通路有关。     

大承气汤对过敏性哮喘小鼠肺组织形态及IgE水平的影响

目的观察大承气汤对过敏性哮喘小鼠肺组织形态学变化、肺指数、脾指数以及总Ig E水平的影响,探讨其相关作用机制。方法采用卵白蛋白致敏加激发的方式建立小鼠过敏性哮喘模型。将20只雌性C57BL/6小鼠随机分为正常组、模型组、大承气汤组和阳性药组,各给药组给予相应药物灌胃。测定各组小鼠肺指数、脾指数,ELISA测定血清Ig E含量,HE染色进行病理观察。结果与正常组比较,模型组小鼠肺指数增加,血清Ig E含量明显升高(P0.01),肺组织出现炎性病理改变;与模型组比较,大承气汤组和阳性药组小鼠肺指数明显降低(P0.05),血清Ig E含量明显降低(P0.01),肺组织形态结构明显改善。结论大承气汤对哮喘小鼠肺部炎症有抑制作用。     

“通腑”对卵清蛋白致敏支气管哮喘小鼠模型的影响

目的:观察支气管哮喘模型小鼠肺部相关病理改变及大承气汤的干预作用,为开展支气管哮喘"从肠论治"效应机制研究,探讨"肺合大肠"脏腑相关联络机制奠定基础。方法:40只C57BL/6小鼠随机分为正常组、模型组、模型给药组及正常给药组,采用卵清蛋白(OVA)致敏激发法建立支气管哮喘小鼠模型。造模第15～21天,正常组、模型组蒸馏水灌胃,模型给药组、正常给药组以大承气汤灌胃,连续7天。观察各组小鼠整体情况和肺组织病理学改变,收集肺支气管肺泡灌洗液(BALF)进行细胞分类计数。结果:OVA致敏哮喘模型小鼠可见剧烈咳嗽、呼吸急促、喘息、打喷嚏、哮鸣音、腹肌抽搐、大小便失禁等症,BALF中淋巴细胞、嗜酸性粒细胞和中性粒细胞比例均明显升高(P<0.01);肺组织病理学存在支气管上皮损坏、肺泡周围充血,伴淋巴细胞浸润等明显改变。经大承气汤从肠干预后,上述症状、体征及病理改变有所减轻。结论:采用OVA致敏法制备的支气管哮喘小鼠模型,存在明显的气道高反应性及炎症性病理改变。通腑法即采用大承气汤通利大肠,能够在一定程度上改善小鼠模型肺部的症状及病理变化,其作用调节机制,有待进一步研究。     

补肾平喘方对过敏性哮喘小鼠气道炎症改善效果的实验研究

目的:研究补肾平喘方对过敏性哮喘小鼠气道炎症的改善效果。方法:腹腔注射卵清蛋白(OVA)制备过敏性哮喘模型小鼠,随机分为补肾平喘方低、高剂量组(15、30g·kg~(-1)·d~(-1))、地塞米松组(1mg·kg~(-1)·d~(-1))、模型组(等体积生理盐水)。OVA攻击诱导致敏期间给与药物干预,连续8周。末次OVA攻击后,测定各组气道阻力、支气管肺泡灌洗液(BALF)炎症细胞计数、γ-干扰素(IFN-γ)、白介素4(IL-4)、IL-5、IL-13、肿瘤坏死因子α(TNF-α)、Ig E水平。行HE、AB-PAS染色分别观察气道炎性细胞浸润及肺组织黏液分泌情况。Western blot检测肺组织中NF-κBp65、IκBα、TLR4、Foxp3蛋白表达。结果:给药干预后,补肾平喘方可显著降低气道阻力及炎症细胞数量,同时可降低IFN-γ、IL-4、IL-5、IL-13、TNF-α、Ig E水平,下调p-NF-κBp65/NF-κBp65、p-IκBα/IκBα与TLR4蛋白表达,上调Foxp3蛋白表达。HE、AB-PAS染色结果显示补肾平喘方可减少炎性细胞浸润,抑制肺组织黏液分泌和杯状细胞增生,且呈剂量依赖性。结论:补肾平喘方可有效改善过敏性哮喘小鼠气道炎症,发挥平喘作用。     

姜黄素对慢性哮喘大鼠气道炎症及p-ERK1/2表达的影响

目的:观察姜黄素对慢性哮喘大鼠肺泡灌洗液中炎症细胞变化及肺组织中细胞外信号调节激酶1/2磷酸化(p-ERK1/2)表达水平表达的影响,探讨姜黄素抑制哮喘大鼠气道炎症和改善气道重塑的作用机理。方法:30只雄性SD大鼠随机分为正常对照组(N组)、哮喘模型组(A组)、姜黄素组(C组)各10只,采用卵蛋白(OVA)等致敏大鼠哮喘模型,观察3组动物哮喘发作症状、气道炎症情况及免疫组化染色后p-ERK1/2表达情况。结果:哮喘模型组大鼠哮喘发作症状最明显,姜黄素组大鼠症状轻,正常对照组无症状。肺泡灌洗液总细胞数及中性粒细胞哮喘模型组明显高于正常对照组和姜黄素组。肺组织石蜡切片免疫组化发现哮喘模型组肺组织中p-ERK1/2吸光度显著高于同时期正常对照组、姜黄素组(均P<0.01)。结论:姜黄素可抑制哮喘的慢性气道炎症,改善气道重塑,其机制可能与抑制哮喘大鼠ERK1/2的磷酸化有关。     

朝医补肺元汤对哮喘模型小鼠肺组织中p38蛋白激酶表达的影响

目的:探讨朝医补肺元汤对小鼠哮喘模型肺组织中p38蛋白激酶表达的作用及其可能机制。方法:雄性BALB/c小鼠40只随机分成5组。支气管肺泡灌洗液(BALF)中IL-5、IL-13的含量采用酶联免疫吸附法(ELISA)测出,并对支气管肺泡灌洗液中炎症细胞的病理学改变进行观察。应用免疫蛋白质印迹(Western blot)测小鼠肺组织中磷酸化的p38MAPK表达作用强弱。结果:相较于正常对照组,哮喘模型组小鼠BALF中IL-5、IL-13以及肺组织中的磷酸化p38MAPK表达增强(P0.05)。相比较于小鼠哮喘模型组,朝医补肺元汤低、高剂量组小鼠肺泡灌洗液中的IL-5、IL-13、肺组织磷酸化p38MAPK表达水平显著降低(P0.05)。综上可证明朝医补肺元汤能显著改善哮喘小鼠肺组织的病理学上的改变。结论:朝医补肺元汤显著治疗哮喘的功效密切相关于阻碍哮喘小鼠p38MAPK信号通路的表达。     

隐丹参酮通过抑制p38 MAPK/NF-κB通路改善哮喘气道炎症

目的探究隐丹参酮(CTS)对哮喘小鼠气道炎症的影响,并探讨其可能的作用机制。方法将50只雌性BALB/c小鼠随机分为5组:生理盐水对照组(Control)、OVA哮喘组(OVA)、CTS低剂量组(CTS 50)、CTS高剂量组(CTS 100)、地塞米松阳性对照组(DEX),每组10只。建立卵清蛋白(Ovalbumin,OVA)诱导的哮喘小鼠模型,分别用50 mg·kg^-1、100 mg·kg^-1 CTS及10 mg·kg^-1地塞米松腹腔注射处理各组小鼠,对照组用等量生理盐水代替。末次激发24 h后处死小鼠,取支气管肺泡灌洗液(BALF)及肺脏。以Diff-Quick染色对小鼠BALF中炎症细胞进行分类计数;ELISA法检测小鼠BALF中IL-4、IL-5、IL-13含量;小鼠肺石蜡包埋,切片,行HE和PAS染色,观察小鼠肺组织的病理学改变;Western Blot观察核因子(NF)-κB p65表达水平,以及IkB-α、p38 MAPK磷酸化水平。结果 CTS显著减少哮喘小鼠BALF中炎症细胞数量,并降低小鼠BALF中IL-4、IL-5、IL-13含量(P<0.05);CTS显著抑制肺组织中炎症细胞浸润、杯状细胞增生及黏液分泌;CTS抑制NF-κB p65活化并抑制IkB-α、p38 MAPK磷酸化(P<0.05)。结论 CTS可抑制哮喘小鼠气道炎症,其机制可能与抑制p38 MAPK/NF-κB信号通路有关。     

隐孔菌发酵物对脾虚证哮喘小鼠气道高反应性及炎症的影响

目的建立脾虚证哮喘小鼠模型,观察隐孔菌发酵物(CVFS)对脾虚证哮喘小鼠气道高反应性及炎症的影响。方法以卵白蛋白(OVA)致敏 饮食不节 劳倦过度伤脾法建立脾虚证哮喘小鼠模型;测定小鼠的肺阻力(RL)和支气管-肺泡灌洗液(BALF)中的炎症细胞,观察肺组织和免疫器官脾脏的病理变化。结果脾虚证哮喘小鼠的气道高反应性、BALF中的嗜酸性粒细胞数目,肺组织嗜酸性粒细胞炎性病理变化以及脾脏指数与单纯哮喘小鼠比较有明显差异(P<0.05)。CVFS能明显改善单纯哮喘小鼠和脾虚证哮喘小鼠由乙酰甲胆碱(MCH)诱导的气道高反应性,减少BALF中的嗜酸性粒细胞数目,以及改善肺组织嗜酸性粒细胞炎性病理变化,而对脾虚证哮喘小鼠作用更为明显。CVFS能明显增加脾虚证哮喘小鼠脾脏指数,而对单纯哮喘小鼠的脾脏指数无明显影响。结论OVA致敏 饮食不节 劳倦过度伤脾法可建立脾虚证哮喘小鼠模型;CVFS可明显改善脾虚症状,抑制脾虚证哮喘小鼠的气道高反应性和炎症反应,提示CVFS可用于临床脾虚证哮喘的治疗。     

差异蛋白质组学法探索大承气汤优化方治疗便秘小鼠的生物学基础

目的:应用差异蛋白质组学方法探索大承气汤优化方治疗便秘小鼠的生物学基础。方法:实验动物分为正常组、模型组及大承气汤优化方组。模型组、大承气汤优化方组小鼠按50 mg·kg~(-1)灌胃给予复方地芬诺酯混悬液以制备便秘模型,正常组小鼠则给予等量生理盐水。大承气汤优化方组按31 g·kg~(-1)灌胃给予大承气汤优化方药液,正常组及模型组小鼠则给予等量生理盐水。完成药效指标检测后,处死动物,称取小鼠大肠组织,提取蛋白样品,经纳升级高效液相色谱联用线性离子阱/静电场轨道阱高分辨组合式质谱(Nano LC-LTQ Orbitrap Elite)系统分析检测,Protein Discovery软件进行蛋白质搜库,Sieve v2.1软件对所有样本蛋白进行相对定量分析。结果:与模型组相比,大承气汤优化方组小鼠的肠组织蛋白表达上调或下调且与正常组变化方向一致的有77个。经文献检索分析表明,以上蛋白生物学功能一方面集中于促进糖脂代谢、三羧酸循环、生物氧化及能量代谢等,由此增加机体对大肠蠕动的供能,另一方面表现为增强肠道平滑肌的收缩功能,以促进肠道蠕动,缓解便秘。结论:差异蛋白质组学法找出的相关蛋白靶点及其涉及的生物体调控通路极可能是大承气汤优化方治疗便秘小鼠的生物学基础。     

Effect of Kuwanon G Isolated from the Root Bark of Morus alba on Ovalbumin‐induced Allergic Response in a Mouse Model of Asthma

The root bark of Morus alba L. (Mori Cortex Radicis; MCR) is traditionally used in Korean medicine for upper respiratory diseases. In this study, we investigated the antiasthmatic effect of kuwanon G isolated from MCR on ovalbumin (OVA)‐induced allergic asthma in mice. Kuwanon G (1 and 10 mg/kg) was administered orally in mice once a day for 7 days during OVA airway challenge. We measured the levels of OVA‐specific IgE and Th2 cytokines (IL‐4, IL‐5, and IL‐13) in the sera or bronchoalveolar lavage (BAL) fluids and also counted the immune cells in BAL fluids. Histopathological changes in the lung tissues were analyzed. Kuwanon G significantly decreased the levels of OVA‐specific IgE and IL‐4, IL‐5, and IL‐13 in the sera and BAL fluids of asthma mice. Kuwanon G reduced the numbers of inflammatory cells in the BAL fluids of asthma mice. Furthermore, the pathological feature of lungs including infiltration of inflammatory cells, thickened epithelium of bronchioles, mucus, and collagen accumulation was inhibited by kuwanon G. These results indicate that kuwanon G prevents the pathological progression of allergic asthma through the inhibition of lung destruction by inflammation and immune stimulation. Copyright © 2014 John Wiley & Sons, Ltd.     

三拗汤对哮喘小鼠变应性气道炎症的影响及其成分分析

目的:评价三拗汤对哮喘小鼠变应性气道炎症的影响,并对全方成分进行分析.方法:BALB/c小鼠60只,随机分为正常组、模型组、三拗汤高、中、低剂量(7.2,3.6,1.8 g·kg-1)组、地塞米松组(0.75 mg·kg-1).各组小鼠(除空白组)于第1,8天腹腔、皮下分别给予0.1 mL的致敏液(0.2 mL致敏液含卵蛋白OVA 0.1 mg,Al(OH)3 0.02 mg),第15～28天各组(除空白组)给予5％的OVA雾化,每次雾化20 min,每次雾化前30 min各组小鼠按体重给予相应的药物;空白组以等体积生理盐水代替致敏液,且生理盐水雾化相同的时间.相应的药物治疗2周后,取血做嗜酸细胞计数(EOS),取肺泡灌洗液(BALF)做细胞分类计数.采用超高效液相-四级杆串联飞行时间质谱(UPLC-QTOFMS)鉴定其化学成分.结果:三拗汤中剂量组使哮喘小鼠血中EOS的含量明显的降低(P＜0.01),三拗汤高、低剂量组使哮喘小鼠血中的EOS含量有所降低(P＜0.05),三拗汤高、中、低剂量使BALF中的EOS明显下降(P＜0.01,P＜0.05),从三拗汤全方中初步鉴定了22个化合物.结论:三拗汤对哮喘小鼠变应性气道炎症有明显的抑制作用,其全方主要化学成分为生物碱、黄酮、皂苷成分,这些化学组分与其发挥抗哮喘小鼠变应性气道炎症有密切的关系.     

平喘颗粒对哮喘小鼠肺组织MMP-9和TIMP-1水平的影响

目的观察平喘颗粒对哮喘小鼠肺组织基质金属蛋白酶-9(MMP-9)和基质金属蛋白酶组织抑制剂-1(TIMP-1)水平的影响。方法40只BALB/c小鼠,随机分为4组,分别是对照组、哮喘组、平喘颗粒组、普米克令舒组,每组10只。对照组腹腔注射及雾化吸入等体积生理盐水代替OVA激发,其他3组腹腔注射及雾化吸入卵清蛋白(OVA)造成慢性哮喘动物模型。从第1次雾化激发的当天开始,平喘颗粒组每天灌胃给予平喘颗粒药液,持续给药8周,激发阶段则每次激发前1 h灌胃;对照组和哮喘组给予等体积的生理盐水灌胃,灌胃时间同平喘颗粒组。普米克令舒组给予普米克令舒雾化吸入,每次30 min,雾化时间同平喘颗粒组。取各组小鼠肺组织切片行Masson染色,光镜下检测肺组织病理改变情况,采用计算机图像分析系统测定支气管基底膜周径(Pbm)、气道平滑肌面积(WAm)和支气管总面积(WAt)。酶联免疫吸附测定(ELISA)法检测肺组织中MMP-9和TIMP-1的表达水平。结果与对照组比较,哮喘组小鼠WAm/Pbm、WAt/Pbm明显增高(P<0.05),肺组织中MMP-9、TIMP-1的表达水平明显增高(P<0.05);平喘颗粒组和普米克令舒组上述指标较哮喘组均明显下降(P<0.05)。结论平喘颗粒可以减轻哮喘小鼠肺组织病理学改变,改善气道重塑,其机制可能与抑制MMP-9和TIMP-1的表达有关。     

Xiaoqinglong decoction reduces dendritic cell differentiation and regulates the Th1/Th2 balance in a mouse model of allergic asthma

BackgroundXiaoqinglong decoction (XQLD) is a classic Chinese medicinal formula that is widely used to treat allergic asthma. Recently, the use of XQLD to treat allergic asthma has inspired research to determine its mechanism of action. Because dendritic cells (DCs) and the T helper 1 (Th1)/Th2 cytokine balance play important roles in allergic asthma, the present work aimed to assess how these immune system components are affected by XQLD.MethodsThirty-six female BALB/C mice were randomly divided into three groups: an ovalbumin-based allergic asthma model group, a XQLD treatment group, and a control group. Histology was performed with haematoxylin and eosin staining and immunohistochemical staining. Bronchoalveolar lavage fluid and blood were collected from the animals and used to analyze the composition of inflammatory cells and expression levels of the cytokines interleukin (IL)-5 and IL-13. The thymic stromal lymphopoietin (TSLP) protein expression was assessed by western blot analysis, and the Gata3 and Tbx21 mRNA levels were assessed by polymerase chain reaction.ResultsCompared with the OVA group, the levels of TSLP expression, IL-5, IL-13, and immunoglobulin E in the XQLD group were lower (all P < .01). The level of IL-4-expressing cells (Th2 cells) was lower (P = .0013), and the percentage of IFN-γ-expressing cells (Th1 cells) was higher in the XQLD group compared with those in the OVA group (P = .0065). In addition, XQLD increased the expression of Tbx21 mRNA and decreased the expression of Gata3 mRNA in the lungs compared with the OVA group (both P < .01).ConclusionThese findings suggest that XQLD may ameliorate the course of allergic asthma by regulating the Gata3/Tbx21 balance and inhibiting TSLP expression, changes which are indicative of an altered Th1/Th2 balance. Thus, the clinical effectiveness of XQLD in treating allergic asthma may be due to its regulation of Th1/Th2 balance.     

Effects of taraxasterol on ovalbumin-induced allergic asthma in mice

Ethnopharmacological relevance

Taraxasterol was isolated from the Chinese medicinal herb Taraxacum officinale which has been frequently used as a remedy for inflammatory diseases. In the present study, we determined the in vivo protective effect of taraxasterol on allergic asthma induced by ovalbumin (OVA) in mice.

Materials and methods

Mice were sensitized and challenged with OVA, and were orally treated daily with taraxasterol at 2.5, 5 and 10 mg/kg from day 23 to 27 after sensitization. The number of inflammatory cells in bronchoalveolar lavage fluid (BALF) was determined. Th2 cytokine interleukin-4 (IL-4), interleukin-5 (IL-5), interleukin-13 (IL-13) production in BALF and OVA-specific immunoglobulin E (IgE) production in sera were measured using ELISA. Histological changes in lung tissues were examined using hematoxylin and eosin (H&E) and periodic acid-Schiff staining (PAS). Airway hyperresponsiveness (AHR) to inhaled methacholine was assessed.

Results

Taraxasterol dramatically decreased the total inflammatory cell and main inflammatory cell counts, reduced the production of Th2 cytokine IL-4, IL-5, IL-13 in BALF and OVA-specific IgE in sera, and suppressed AHR in a dose-dependent manner. Histological studies demonstrated that taraxasterol substantially suppressed OVA-induced inflammatory cells infiltration into lung tissues and goblet cell hyperplasia in airways.

Conclusions

This finding suggests that taraxasterol protects against OVA-induced allergic asthma in mice.     

Panax ginseng ameliorates airway inflammation in an ovalbumin-sensitized mouse allergic asthma model

Ethnopharmacological relevance

Panax ginseng (PG) is a medicinal herb that has been used to treat various immune diseases including asthma and COPD. In this study, we investigated the inhibitory mechanism of PG on asthma parameters in mice.

Materials and methods

BALB/c mice were sensitized with 20 μg/200 μl OVA adsorbed on 1.0 mg/50 μl aluminum hydroxide gel adjuvant by i.p. injection on days 0 and 14. Mice were then challenged with 5% OVA in PBS to the nose for 30 min once a day for 3 days, from day 20 until day 22, using a nebulizer. PG (20 mg/kg) or vehicle was administrated by i.p. injection once a day 10 min before every OVA challenge for 3 days. The recruitment of inflammatory cells into bronchoalveolar lavage fluid or lung tissues was measured. The expression of EMBP, Muc5ac, CD40, and CD40 ligand (CD40L) in lung tissues was investigated. In addition, the cytokines and mitogen activated protein (MAP) kinases were measured by RT-PCR and Western blot.

Results and conclusions

PG restored the expression of EMBP, Muc5ac, CD40, and CD40L, as well as the mRNA and protein levels of interleukin (IL)-1β, IL-4, IL-5, and tumor necrosis factor (TNF)-α. In addition, PG inhibited the numbers of goblet cells and further small G proteins and MAP kinases in bronchoalveolar lavage cells and lung tissues increased in ovalbumin-induced allergic asthma in mice. These results suggest that PG may be used as a therapeutic agent in asthma, based on reductions of various allergic responses.     

龙脷平喘膏抗哮喘大鼠气道炎症作用及机制

目的:探讨龙脷平喘膏对发作期小儿哮喘气道炎症的影响。方法:48只大鼠按体重均衡随机分为空白对照组、模型组、地塞米松组(1 mg·kg-1)、龙脷平喘膏高、中、低剂量组(74.8,37.4,18.7 g·kg-1),每组8只。采用卵清蛋白(OVA)复制哮喘大鼠模型,连续给药1周,记录大鼠过敏性鼻炎症状,取鼻黏膜和肺组织,观察鼻黏膜及肺组织病理形态变化,并检测肺组织炎症细胞凋亡率和原癌基因Fas(Fas mRNA),B细胞淋巴瘤/白血病2基因(Bcl-2 mRNA)的表达。结果:除空白组外,其他各组在引发过敏性哮喘的同时均诱发了不同程度的过敏性鼻炎症状,且模型组鼻黏膜和肺组织均见嗜酸粒细胞浸润及相似的病理形态学改变;与空白组比较,模型组大鼠搔鼻和喷嚏的次数显著增多(P<0.01);与模型组比较,龙脷平喘膏能明显减少哮喘大鼠搔鼻和喷嚏的次数(P<0.01)。与空白组比较,模型组大鼠肺组织中炎症细胞凋亡率显著降低(P<0.01);与模型组比较,龙脷平喘膏高、中剂量组大鼠肺组织中炎症细胞凋亡率明显升高(P<0.05),且肺组织中促炎症细胞凋亡的调控基因Fas mRNA阳性表达率显著升高(P<0.01),抑制炎症细胞凋亡的调控基因Bcl-2 mRNA阳性表达率则显著下降(P<0.01)。结论:龙脷平喘膏能明显抑制哮喘大鼠气道炎症,机制可能与其逆转Fas/Bcl-2失衡,促进炎症细胞凋亡有关。