咳喘凝胶贴膏穴位敷贴对支气管哮喘大鼠炎症因子的影响

摘要：目的:通过观察支气管哮喘模型大鼠炎症因子的变化,探讨咳喘凝胶贴膏对支气管哮喘的治疗作用。方法:50只SD大鼠随机分为正常对照组、哮喘模型组、地塞米松组、咳喘凝胶贴膏药物组、假穴位组,每组10只。采用卵蛋白（OVA）致敏和雾化吸入激发的方法建立支气管哮喘大鼠模型。建模成功后,正常对照组大鼠和哮喘模型组给予生理盐水灌胃;地塞米松组大鼠给予地塞米松混悬液1 mg·kg-1·d-1灌胃;咳喘凝胶贴膏组及假穴位敷贴组于肺腧、肾腧穴分别给予药物和空白基质进行穴位给药,1次/d,每侧面积约为2 cm×2 cm,共2周。在末次激发24 h后收集支气管肺泡灌洗液（BALF）,光学显微镜下进行大鼠肺泡灌洗液嗜酸性粒细胞（EOS）计数,采用酶联免疫法检测大鼠白细胞介素-17（IL-17）、白细胞介素-1（IL-1β）、白细胞介素-13（IL-13）水平。结果:OVA成功诱导支气管哮喘模型;与正常对照组相比,模型组和假穴位组大鼠EOS计数、IL-17、IL-1β、IL-13水平均显著升高（P<0.05或P<0.01）;与模型组相比,地塞米松组、咳喘凝胶贴膏药物组均能显著降低EOS数量、IL-17、IL-1β、IL-13水平（P<0.05或P<0.01）;地塞米松组与咳喘凝胶贴膏药物组各指标比较差异无统计学意义（P>0.05）。结论:咳喘凝胶贴膏可降低OVA诱发哮喘大鼠EOS数量,影响IL-17、IL-1β、IL-13表达水平。     

孟鲁司特与桂龙咳喘宁联合治疗支气管哮喘实验性研究

目的研究孟鲁司特与桂龙咳喘宁对支气管哮喘小鼠模型的影响。方法将50只实验小鼠随机分为正常组、哮喘模型组、孟鲁司特组、桂龙咳喘宁组及联合用药组,以卵白蛋白致敏法制作小鼠哮喘模型,以ELISA法测定各组小鼠血清IL-4、IL-10含量。结果哮喘模型组血清中IL-4的含量明显大于正常组(P<0.05),IL-10含量明显小于正常组(P<0.05),孟鲁司特组与联合用药组均较哮喘模型组IL-4、IL-10含量差异有统计学意义(P<0.05),桂龙咳喘宁组IL-4含量均较哮喘模型组有明显升高(P<0.05),IL-10含量差异无统计学意义(P>0.05)。结论孟鲁司特与桂龙咳喘宁均能显著抑制支气管哮喘小鼠模型血清IL-4含量,二者联用可对IL-4、IL-10含量有显著影响。     

地塞米松对哮喘模型大鼠肺组织病理变化和TGF-β1表达的影响

目的:探讨哮喘时肺组织炎症、中性粒细胞(PMN)、肺泡Ⅱ型(AT-Ⅱ)细胞等的病理改变和转化生长因子-β1(TGF-β1)的表达及地塞米松对其的影响.方法:建立哮喘大鼠模型,支气管肺泡灌洗液(BALF)行细胞计数,光镜、电镜观察肺组织病理改变,免疫组化法检测肺组织TGF-β1的表达.结果:BALF中A组细胞总数、EOS计数显著性高于C组(P<0.01),D组显著性高于C组但低于A组(均P<0.01).肺组织中A组PMN计数显著性高于C组(P<0.01),D组显著性高于A组(P<0.01).A组AT-Ⅱ细胞变性、坏死、崩解、板层体空泡化现象.TGF-β1的表达水平在A组显著性高于C组(P<0.01),D组显著性高于C组但低于A组(分另为P<0.01,0.05).结论:哮喘大鼠肺组织炎症细胞浸润、气道黏膜损伤、AT-Ⅱ细胞损伤、表达水平增加;地塞米松可减少上述病理改变,但对肺组织中PMN数目有增加作用,可能会加重对肺组织的损伤.     

天贝止喘汤对支气管哮喘小鼠Th1/Th2影响的研究

目的观察天贝止喘汤对支气管哮喘小鼠肺组织、血清Ig E、支气管肺泡灌洗液IL-4、IL-10、IL-12和TNF-α影响,研究天贝止喘汤保护哮喘小鼠可能的机制。方法 70只健康SPF级雌性BALB/c小鼠适应性饲养后,分为7组(空白对照组、哮喘模型组、天贝止喘汤低剂量组、天贝止喘汤中剂量组、天贝止喘汤高剂量组、小青龙组、地塞米松组),10只/组。卵清白蛋白建立小鼠支气管哮喘气道炎症模型,取材后观察肺组织变化、测定血清Ig E、支气管肺泡灌洗液IL-4、IL-10、IL-12和TNF-α水平变化。结果空白组肺组织无明显炎症细胞浸润、肺组织及气道壁形态结构完整;模型组肺组织有大量炎症细胞浸润、肺组织及气道壁增厚明显,结构受损,其余各药物治疗组较模型组均有不同程度改善。与空白组相比,模型组和各药物治疗组血清Ig E水平、支气管肺泡灌洗液IL-4、TNF-α水平显著升高(P<0.05),IL-10、IL-12水平显著降低(P<0.05);与模型组相比,各药物治疗组血清Ig E水平、支气管肺泡灌洗液IL-4、TNF-α水平显著降低(P<0.05),IL-10、IL-12水平显著升高(P<0.05)。结论天贝止喘汤可能通过调节Th1/Th2平衡,调节炎性细胞因子水平保护哮喘小鼠,高剂量效果更明显。     

刘世琼教授"冬病夏治"治疗小儿咳嗽48例

目的:观察“咳喘宁”贴膏治疗小儿咳嗽的临床疗效。方法:选择2001年至2004年收治的小儿咳嗽病例48例,每年夏季“三伏天”时采用“咳喘宁”贴膏贴敷穴位,并随证加减。结果:经13年的治疗,取得明显疗效,其中显效23例,有效18例,无效7例,总有效率85.42%。结论:“咳喘宁”贴膏具有止咳祛痰清肺平喘作用可提高患儿机体正气从而达到治疗小儿咳嗽之目的。     

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。     

中药穴位贴敷治疗支气管哮喘效果评价及护理干预

目的：评价中药穴位贴敷治疗支气管哮喘的效果。方法将我院2011年6月－2013年9月共62例支气管哮喘患者随机分为观察组32例和对照组30例,2组均予常规治疗,观察组加用中药穴位贴敷治疗,于治疗3个疗程后评定疗效。结果观察组与对照组治疗效果比较差异有显著性（χ2＝5.92,P＜0.05）。结论中药穴位贴敷能提高支气管哮喘患者的治疗效果。     

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。     

慢性轻度不可预见性应激对支气管哮喘大鼠的影响

目的 观察慢性轻度不可预见性应激对支气管哮喘大鼠哮喘病情的影响.方法 通过对哮喘组及实验组大鼠腹腔注射卵蛋白,并雾化吸入卵蛋白制备支气管哮喘模型.在雾化吸入卵蛋白后对实验组进行连续28 d的慢性轻度不可预见性应激.此后以无创小动物呼吸功能测量仪检测大鼠呼吸功能、HE染色观察肺组织病变、并支气管灌洗液中细胞数量及分类.结果 ①与正常组比较,哮喘组呼吸功能降低(P<0.05);与哮喘组比较,哮喘组大鼠呼吸功能进一步降低(P<0.05).②与正常组比较,哮喘组大鼠支气管灌洗液中白细胞总数及嗜酸性粒细胞均显著升高(P<0.05);与哮喘组比较,哮喘组大鼠支气管灌洗液中自细胞总数及嗜酸性粒细胞均显著升高(P<0.05).③与哮喘组大鼠比较,实验组大鼠支气管壁上皮细胞较哮喘组排列更加紊乱,部分结构破坏,白细胞浸润较哮喘组更加显著,肺泡失去正常形态.结论 慢性轻度不可预见性应激可以通过加重哮喘病情,临床工作中应注重对哮喘患者进行心理疏导、避免心理应激.     

金匮肾气汤结合冬病夏治穴位贴敷治疗支气管哮喘缓解期的临床效果观察

目的:分析对支气管哮喘缓解期采用金匮肾气汤结合冬病夏治穴位贴敷治疗的临床疗效.方法:选取我院2015年1月～2016年12月收治的支气管哮喘缓解期患者80例,随机分成两组,对照组(n=40)采用常规西药治疗,观察组(n=40)采用金匮肾气汤联合冬病夏治穴位贴敷,比较两组临床疗效及肺功能改善情况.结果:观察组总有效率为87.5％,高于对照组的67.5％;两组治疗前FEV1比较无明显差异(P>0.05),治疗后观察组明显高于本组治疗前与对照组(P<0.05).结论:对支气管哮喘缓解期采用金匮肾气汤结合冬病夏治穴位贴敷治疗临床疗效优良,有推广价值.     

Inhibitory effect of Platycodi Radix on ovalbumin-induced airway inflammation in a murine model of asthma

Asthma is a chronic inflammatory disease of the airways characterized by an associated increase in airway responsiveness. In this study, we investigated the inhibitory effect of an aqueous extract from the root of Platycodi Radix (Changkil: CK) on airway inflammation in a murine model of asthma. Mice were sensitized and challenged by ovalbumin (OVA) inhalation to induce chronic airway inflammation and airway remodeling. CK markedly decreased the number of infiltrated inflammatory cells and the levels of Th1 and Th2 cytokines and chemokines compared with those in the OVA-induced group. In addition, CK reduced OVA-specific IgE levels in bronchoalveolar lavage (BAL) fluid. Based on lung histopathological studies, inflammatory cell infiltration and mucus hypersecretion were inhibited by CK administration compared to that in the OVA-induced group. Lung weight was reduced after CK administration. Also, increased generation of ROS in BAL fluid, as well as NF-κB nuclear translocation, by inhalation of OVA was diminished by CK. Moreover, CK reduced the OVA-induced upregulation of matrix metalloproteases activity. These findings indicate that oxidative stress may play a crucial role in the pathogenesis of bronchial asthma induced by OVA and that CK may be useful as an adjuvant therapy for the treatment of bronchial asthma.     

Effects of astilbic acid on airway hyperresponsiveness and inflammation in a mouse model of allergic asthma

Bronchial asthma is characterized by chronic lung inflammation, airway hyperresponsiveness (AHR), and airway remodeling. Astilbic acid, extracted from the medicinal herb Astilbe chinensis, is used as a headache remedy in traditional medicine and has anti-pyretic and analgesic effects. However, the effect of astilbic acid on asthma remains to be established. In the present study, we therefore examined the effect of astilbic acid in a mouse model in which asthma was established by sensitization and challenge with ovalbumin (OVA). Astilbic acid inhibited OVA-induced AHR to inhaled methacholine and significantly suppressed the levels of T-helper 2-type cytokines (including IL [interleukin]-4, IL-5, and IL-13) and inflammatory cells (including eosinophils) in bronchoalveolar lavage (BAL) fluid. Histochemical analysis revealed reduced goblet cell hyperplasia and mucus production, as well as attenuated eosinophil-rich leukocyte infiltration, in the astilbic acid-treated group, compared with OVA-challenged mice. Moreover, the compound significantly inhibited synthesis of IL-4-, IL-5-, IL-13-, IL-17-, and eotaxin-encoding mRNA following asthma induction in lung tissue, in addition to suppressing the immunoglobulin E (IgE) response to asthma in both BAL fluid and serum. Our results indicate that astilbic acid has great potential as a therapeutic candidate for the treatment of asthma.     

环孢素A气雾吸入对哮喘大鼠气道炎症的影响

目的研究环孢素A(CsA)气雾吸入对抗原诱导的大鼠过敏性气道炎症的作用。方法用卵白蛋白(OA)致敏大鼠,2周后气雾吸入CsA(5，10，20 g·L^-1),每天1次，连续7 d。大鼠致敏后d 20和d 21用OA(10 g·L^-1，每天1次)攻击，观察第2次OA攻击24 h后支气管肺泡灌洗液及外周血中嗜酸性粒细胞的数量和支气管肺组织病理学改变情况，测定支气管肺泡灌洗液中TNF-α含量。结果CsA气雾吸入能明显降低支气管肺泡灌洗液及外周血中嗜酸性粒细胞的数量，减轻肺组织中炎症细胞特别是嗜酸性粒细胞的浸润,减轻组织水肿及上皮损伤等气道炎症状况,降低支气管肺泡灌洗液中TNF-α含量。结论CsA气雾吸入对大鼠过敏性气道炎症具有抑制作用，其作用机制与细胞因子TNF-α释放减少有关。     

中药雾化治疗对慢阻肺大鼠气道炎症的研究

目的观察中药雾化吸入对慢性阻塞性肺疾病(COPD)大鼠模型肺炎性细胞及炎症介质IL-8、TNF-a含量变化的影响及意义,探讨其对COPD的防治机制。方法采用"烟熏复合木瓜蛋白酶雾化吸入法"复制COPD大鼠模型,随机分为治疗组、模型组、对照组。治疗组给予中药雾化吸入,模型组及对照组给予生理盐水雾化吸入,疗程为4周。观察肺泡灌洗液细胞学分类、血清IL-8及TNF-a含量、肺组织的病理变化。结果中药组肺泡灌洗液炎性细胞计数及血清炎性介质IL-8、TNF-a含量低于模型组(P<0.05);气管和支气管黏膜上皮脱落、气管软骨损毁、支气管腔内炎性细胞渗出等较模型组明显减轻。结论中药雾化能减轻支气管肺组织炎性细胞在肺内聚集,抑制炎性介质IL-8、TNF-a的产生,对COPD大鼠肺具有保护作用。     

S-Allyl cysteine reduces eosinophilic airway inflammation and mucus overproduction on ovalbumin-induced allergic asthma model

S-Allyl cysteine (SAC) is an active component in garlic and has various pharmacological effects, such as anti-inflammatory, anti-oxidant, and anti-cancer activities. In this study, we explored the suppressive effects of SAC on allergic airway inflammation induced in an ovalbumin (OVA)-induced asthma mouse model. To induce asthma, BALB/c mice were sensitized to OVA on days 0 and 14 by intraperitoneal injection and exposed to OVA from days 21 to 23 using a nebulizer. SAC was administered to mice by oral gavage at a dose of 10 or 20 mg/kg from days 18 to 23. SAC significantly reduced airway hyperresponsiveness, inflammatory cell counts, and Th2 type cytokines in bronchoalveolar lavage fluid induced by OVA exposure, which was accompanied by reduced serum OVA-specific immunoglobulin E. In histological analysis of the lung tissue, administration of SAC reduced inflammatory cell accumulation into lung tissue and mucus production in airway goblet cells induced by OVA exposure. Additionally, SAC significantly decreased MUC5AC expression and nuclear factor-κB phosphorylation induced by OVA exposure. In summary, SAC effectively suppressed allergic airway inflammation and mucus production in OVA-challenged asthmatic mice. Therefore, SAC shows potential for use in treating allergic asthma.     

Anthocyanins inhibit airway inflammation and hyperresponsiveness in a murine asthma model.

Asthma is a common chronic inflammatory disease regulated by coordination of T-helper cell type 2 (Th2) cytokines and inflammatory signal molecules. Additionally, oxidative stress may play an important role in airway inflammation such as eosinophilia, mucus hypersecretion, and airway hyperresponsiveness (AHR). In the present report, we investigated whether anthocyanins would reduce airway inflammation in a mouse asthma model immunized and challenged with ovalbumin (OVA). OVA inhalation elicited inflammatory responses characterized by eosinophilia and increased lipid hydroperoxide (LPO) in bronchoalveolar lavage (BAL) fluid, enhanced pause (Penh), increased glycoprotein and proliferating cell nuclear antigen (PCNA) expressions in mucus hypersecretion, and an increased expression of various cytokines and cyclooxygenase (COX) 2 in lung tissues. All parameters were attenuated in a dose-dependant manner by the administration of anthocyanins. These results suggest that anthocyanins may attenuate the development of asthma by downregulating Th2 cytokines, proinflammatory cytokines, and COX-2. Our findings suggest that anthocyanins have positive contributions as a dietary supplement for the prevention of asthma.     

Continued inhalation of lidocaine suppresses antigen-induced airway hyperreactivity and airway inflammation in ovalbumin-sensitized guinea pigs

It is unclear whether inhaled lidocaine is effective against airway hyperreactivity and inflammation in asthma. The aim of this study was to investigate the effects of inhaled lidocaine on airway hyperreactivity and inflammation. Airway reactivity to inhaled histamine, cellular composition of bronchoalveolar lavage (BAL) fluid, plasma substance P (SP), and isolated lung tissue were evaluated in ovalbumin (OVA)-sensitized guinea pigs 7 days after OVA challenge. The effects of inhaled lidocaine on this model were also evaluated. Treatment with lidocaine was administered in two fashions: as single inhalation or inhalation bid for 7 consecutive days, for comparison with a saline-inhaled control group. Airway hyperreactivity to histamine, increase in number of total cells and increased proportion of eosinophils in BAL fluid, and marked eosinophil infiltration in airway walls were noted even 7 days after OVA challenge in the control group. Plasma SP level was also significantly increased. Although treatment with single lidocaine inhalation did not affect airway hyperreactivity, continued inhalation (bid for 7 days) attenuated airway hyperreactivity. Continued, but not single, inhalation of lidocaine also suppressed infiltration of eosinophils in BAL fluid and in airway walls. In addition, plasma SP levels were significantly reduced by continued but not by single inhalation. It appears possible that lidocaine when inhaled suppresses eosinophilic inflammation of the airway and SP-induced neurogenic inflammation, leading to alleviation of airway hyperreactivity.     

Evodiamine protects against airway remodelling and inflammation in asthmatic rats by modulating the HMGB1/NF-κB/TLR-4 signalling pathway

ContextEvodiamine, which is isolated from Evodia rutaecarpa (Rutaceae), possess strong anti-inflammatory, immunomodulatory, and antibacterial properties.ObjectiveThe protective effects of evodiamine in asthma were evaluated.Materials and methodsThirty-two Sprague-Dawley (SD) rats were used, asthma was induced by injecting intraperitoneally with a mixture of Al(OH)₃ (100 mg) and ovalbumin (OA; 1 mg/kg), further exposing them to a 2% OA aerosol for 1 week. All animals were divided into four groups: control, asthma, and evodiamine 40 and 80 mg/kg p.o. treated group. Serum levels of inflammatory cytokines, interferon gamma (IFN-γ), and immunoglobulin E (IgE) and infiltrations of inflammatory cells in the bronchoalveolar lavage fluid (BALF) of the animals were determined. The thickness of the smooth muscle layer and airway wall in the intact small bronchioles of asthmatic rats was examined as well.ResultsCytokine levels in the serum and BALF were lower in the evodiamine-treated group than in the asthma group. Evodiamine treatment reduced IgE and IFN-γ levels as well as the inflammatory cell infiltrate in the lung tissue of asthmatic rats. The thickness of the smooth muscle layer and airway wall of intact small bronchioles was less in the evodiamine-treated group than in the asthma group. Lower levels of TLR-4, MyD88, NF-κB, and HMGB1 mRNA in lung tissue were measured in the evodiamine-treated group than in the asthma group.Discussion and conclusionThe effect of evodiamine treatment protects the asthma, as evodiamine reduces airway inflammation and remodelling in the lung tissue by downregulating the HMGB1/NF-κB/TLR-4 pathway in asthma.     

Ganoderma tsugae supplementation alleviates bronchoalveolar inflammation in an airway sensitization and challenge mouse model

Ganoderma tsugae (a Chinese mushroom Songshan lingzhi) cultivated in Taiwan is extensively used in Chinese traditional medicine to treat different diseases. To determine whether G. tsugae has anti-inflammatory effects on bronchoalveolar inflammation in vivo, we investigated the anti-inflammatory effects of G. tsugae products, YK01 and YK07, on bronchoalveolar inflammation using an airway sensitization and challenge mouse model. Female BALB/c mice were weekly sensitized by intraperitoneal injection of ovalbumin (OVA) three times and challenged with aerosolized OVA twice. Differential cell counts of infiltrating leukocytes, inflammatory mediators, cytokines in bronchoalvelor lavage fluid (BALF) of OVA-challenged mice were examined after continuously consuming G. tsugae diets for 5 weeks. We found that supplementation of G. tsugae significantly decreased total infiltrating leukocytes and lymphocyte percentage in BALF in the experimental groups. Supplementation of G. tsugae also significantly reduced inflammatory mediators in BALF including histamine, prostaglandin E2, eotaxin, and protein levels, however the levels of pro-inflammatory cytokines, interleukin (IL)-1beta and IL-6, in BALF did not significantly change. These results suggest that both G. tsugae supplementation diets YK01 and YK07 might alleviate bronchoalveolar inflammation via decreasing the infiltration of inflammatory cells and the secretion of inflammatory mediators into the local tissues of lungs and airways. Further, these results indicate that the relief of bronchoalveolar inflammation in an airway sensitization murine model provides a possible therapeutic application for G. tsugae in allergic asthma.     

Anti-asthmatic effect of schizandrin on OVA-induced airway inflammation in a murine asthma model

Asthma comprises a triad of reversible airway obstruction, bronchial smooth muscle cell hyperreactivity to bronchoconstrictors, and chronic bronchial inflammation. Clinical and experimental findings have established eosinophilia as a sign of allergic disorders. In the present investigation, we evaluated the anti-asthmatic effects of schizandrin and its underlying mechanisms in an in vivo murine asthmatic model. To accomplish this, female BALB/c mice were sensitized and challenged with ovalbumin (OVA), and examined for the following typical asthmatic reactions: increased numbers of eosinophils and other inflammatory cells in bronchoalveolar lavage fluid (BALF); production of Th1 cytokines (such as tumor necrosis factor (TNF)-α in BALF); production of Th2 cytokines (such as interleukin IL-4 and IL-5) in BALF; presence of total and OVA-specific immunoglobulins (Ig)E in serum; presence of oxidative stress; hyperplasia of goblet cells in the lung; and marked influx of inflammatory cells into the lung. Our results collectively show that schizandrin exerts profound inhibitory effects on accumulation of eosinophils into the airways and reduces the levels of IL-4, IL-5, IFN-γ, and TNF-α in BALF. Additionally, schizandrin suppresses the production of reactive oxygen species (ROS) in a dose-dependent manner, and inhibits goblet cell hyperplasia and inflammatory cell infiltration in lung tissue. Thus, schizandrin has anti-asthmatic effects, which seem to be partially mediated by reduction of oxidative stress and airway inflammation, in a murine allergic asthma model. These results indicate that schizandrin may be an effective novel therapeutic agent for the treatment of allergic asthma.