Evaluation of exhaust air dust polymerase chain reaction as a supplement method for soiled bedding sentinel monitoring in specific pathogen free mouse facility using two different individually ventilated cage racks.

Health monitoring is essential for ensuring animal health and reliable research results. Each animal facility should establish adequate health monitoring methods, and microbiological quality control should be implemented through regular health surveillance. Recently, specific pathogen free (SPF) mice have been housed in individually ventilated cage (IVC) racks in the majority of mouse facilities globally, and health monitoring is implemented using a soiled bedding sentinel (SBS). Even though SBS monitoring is a standard method, it has a limitation in that some pathogens are not sufficiently transmitted to the sentinel housed in the IVC. The exhaust air dust polymerase chain reaction (EAD PCR) method has been reported to be a reliable complementary method to SBS monitoring based on research findings. In Korea, health monitoring programs using EAD PCR have not yet been applied to laboratory animal facilities. The microbiological status of mouse colonies housed in the two IVC racks was compared using SBS and EAD PCR monitoring in our SPF mouse facility. Except for Helicobacter spp. and Staphylococcus aureus, the detection of 16 pathogens did not differ between the two methods. In the detection of Helicobacter spp., EAD PCR was found to be more sensitive than SBS. Helicobacter spp. were not found by SBS, whereas four S. aureus positive samples were detected by either SBS or EAD PCR test. According to our findings, EAD PCR can be used as a supplement to SBS monitoring. Moreover, EAD PCR can reduce the number of animals used, making it a 3R (Replacement, Reduction, Refinement)-consistent method.

Clausena anisata-mediated protection against lipopolysaccharide-induced acute lung injury in mice.

Clausena anisata (Willd.) Hook.f. ex Benth. (CA), which is widely used in traditional medicine, reportedly exerts antitumor, anti-inflammatory and other important therapeutic effects. The aim of the present study was to investigate the potential therapeutic effects of CA in a mouse model of lipopolysaccharide (LPS)-induced acute lung injury (ALI) and in LPS-stimulated RAW 264.7 cells. Male C57BL/6 mice were administered treatments for 3 days by oral gavage. On day 3, the mice were instilled intranasally with LPS or PBS followed 3 h later by oral CA (30 mg/kg) or vehicle administration. In vitro, CA decreased nitric oxide (NO) production and pro-inflammatory cytokines, such as interleukin (IL)-6 and prostaglandin E2 (PGE2), in LPS-stimulated RAW 264.7 cells. CA also reduced the expression of pro-inflammatory mediators, such as cyclooxygenase-2. In vivo, CA administration significantly reduced inflammatory cell numbers in the bronchoalveolar lavage fluid (BALF) and suppressed pro-inflammatory cytokine levels, including tumor necrosis factor-α (TNF-α), IL-6, and IL-1ß, as well as reactive oxygen species production in the BALF. CA also effectively reduced airway inflammation in mouse lung tissue of an LPS-induced ALI mouse model, in addition to decreasing inhibitor κB (IκB) and nuclear factor-κB (NF-κB) p65 phosphorylation. Taken together, the findings demonstrated that CA inhibited inflammatory responses in a mouse model of LPS-induced ALI and in LPS-stimulated RAW 264.7 cells. Thus, CA is a potential candidate for development as an adjunctive treatment for inflammatory disorders, such as ALI.

Copper oxide nanoparticles aggravate airway inflammation and mucus production in asthmatic mice via MAPK signaling.

Copper oxide nanoparticles (CuONPs), metal oxide nanoparticles were used in multiple applications including wood preservation, antimicrobial textiles, catalysts for carbon monoxide oxidation and heat transfer fluid in machines. We investigated the effects of CuONPs on the respiratory system in Balb/c mice. In addition, to investigate the effects of CuONPs on asthma development, we used a murine model of ovalbumin (OVA)-induced asthma. CuONPs markedly increased airway hyper-responsiveness (AHR), inflammatory cell counts, proinflammatory cytokines and reactive oxygen species (ROS). CuONPs induced airway inflammation and mucus secretion with increases in phosphorylation of the MAPKs (Erk, JNK and p38). In the OVA-induced asthma model, CuONPs aggravated the increased AHR, inflammatory cell count, proinflammatory cytokines, ROS and immunoglobulin E induced by OVA exposure. In addition, CuONPs markedly increased inflammatory cell infiltration into the lung and mucus secretions, and MAPK phosphorylation was elevated compared to OVA-induced asthmatic mice. Taken together, CuONPs exhibited toxicity on the respiratory system, which was associated with the MAPK phosphorylation. In addition, CuONPs exposure aggravated the development of asthma. We conclude that CuONPs exposure has a potential toxicity in humans with respiratory disease.

Thuja orientalis reduces airway inflammation in ovalbumin-induced allergic asthma.

Thuja orientalis (TO) may be used as a herbal remedy for the treatment of numerous inflammatory diseases. In the present study, the effects of TO were evaluated on airway inflammation in ovalbumin (OVA)­induced allergic asthma and RAW264.7 murine macrophage cells. The effects of TO on the production of proinflammatory mediators, were determined in RAW264.7 cells that had been stimulated with lipopolysaccharide (LPS). Furthermore, an in vivo experiment was performed on mice that were sensitized to OVA and then received an OVA airway challenge. TO was administered by daily oral gavage at a dose of 30 mg/kg, 21­23 days after the initial OVA sensitization. TO was shown to reduce nitric oxide production and reduce the relative mRNA expression levels of inducible nitric oxide synthase (iNOS), interleukin (IL)­6, cyclooxygenase­2, matrix metalloproteinase (MMP)­9, and tumor necrosis factor­α in RAW264.7 cells stimulated with LPS. In addition, TO markedly decreased the inflammatory cell counts in bronchial alveolar lavage fluid, reduced the levels of IL­4, IL­5, IL­13, eotaxin and immunoglobulin E, and reduced airway hyperresponsivenes, in the OVA sensitized mice. Furthermore, TO attenuated airway inflammation and mucus hypersecretion, induced by the OVA challenge of the lung tissue. TO also reduced the expression of iNOS and MMP­9 in lung tissue. In conclusion, TO exerted anti­inflammatory effects in an OVA­induced allergic asthma model, and in LPS­stimulated RAW264.7 cells. These results suggest that TO may be a useful therapeutic agent for the treatment of inflammatory diseases, including allergic asthma.

Zingiber mioga (Thunb.) Roscoe attenuates allergic asthma induced by ovalbumin challenge.

Zingiber mioga (Thunb.) Roscoe (ZM) is a traditional medicine, used to treat inflammatory diseases. The present study aimed to evaluate the inhibitory effects of ZM on the inflammatory response in lipopolysaccharide (LPS)­stimulated RAW264.7 murine macrophage cells and in a mouse model of ovalbumin (OVA)­induced allergic asthma. Mice received OVA sensitization on day 0 and 14, and were challenged with OVA between days 21 and 23. ZM was administered to the mice at a dose of 30 mg/kg, 1 h prior to OVA challenge. In LPS­stimulated RAW264.7 cells, ZM significantly decreased nitric oxide (NO) and tumor necrosis factor (TNF)­α production in a concentration­dependent manner, and mRNA expression of inducible NO synthase (iNOS), TNF­α and matrix metalloproteinase (MMP)­9 was reduced. In addition, treatment with ZM decreased the inflammatory cell count in bronchoalveolar lavage fluid from the mice, and reduced the expression of interleukin (IL)­4, IL­5, IL­13, eotaxin and immunoglobulin E. ZM also reduced airway hyperresponsiveness in OVA­challenged mice, and attenuated the infiltration of inflammatory cells and mucus production in the airways, with a decrease in the expression of iNOS and MMP­9 in lung tissue. In conclusion, the results of the present study indicate that ZM effectively inhibits inflammatory responses. Therefore, it may be that ZM has potential as a therapeutic agent for use in inflammatory diseases.

Anti-inflammatory effects of methanol extract of Canarium lyi C.D. Dai & Yakovlev in RAW 264.7 macrophages and a murine model of lipopolysaccharide-induced lung injury.

Canarium lyi C.D. Dai & Yakovlev (CL) is a member of the Anacardiaceae family. To the best of our knowledge, no studies on its anti-inflammatory effects have yet been reported. In the present study, we investigated the protective effects of CL on inflammation in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells and LPS-induced acute lung injury (ALI) mice. CL attenuated the production of LPS-stimulated inflammatory mediators such as tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß, and interleukin-6 (IL-6). Furthermore, CL suppressed phosphorylation of the inhibitor κB-α (IκB-α), p38, c-Jun terminal kinase (JNK) and extracellular signal-regulated kinase (ERK), as well as the translocation of the nuclear factor-κB (NF-κB) p65 subunit into the nucleus. For the in vivo efficacy, the effect of CL on a mouse model of LPS-induced acute lung injury was assessed. CL treatment of the mice significantly inhibited the inflammatory cell recruitment and pro-inflammatory cytokine production in bronchoalveolar lavage fluids (BALF). CL-treated mice also showed a marked inhibition of cyclooxygenase-2 (COX-2) and phosphorylation of IκB and p65. In addition, CL attenuated lung histopathological changes in LPS-induced ALI mice. In conclusion, our results suggest that CL is a potential therapeutic candidate for the treatment of inflammatory diseases, including pneumonia.

Callicarpa japonica Thunb. reduces inflammatory responses: a mouse model of lipopolysaccharide-induced acute lung injury.

Callicarpa japonica Thunb. (CJT) is traditionally used as an herbal remedy for the treatment of inflammatory diseases. This study aimed to investigate the anti-inflammatory response of CJT in lipopolysaccharide (LPS)-stimulated RAW264.7 cells and LPS-induced acute lung injury (ALI) in mice. The C57BL/6 mice were administered 30 mg/kg of CJT by oral gavage for 3 days. LPS is applied to animals by intranasal administration 1 h after final CJT treatment. LPS is applied to animals by intranasal administration 1h after final CJT treatment. LPS was delivered intranasally 1h after the final CJT treatment. In the LPS-stimulated RAW264.7 cells, CJT significantly decreased nitric oxide (NO) and interleukin (IL)-6 in a concentration-dependent manner by reducing inducible NO synthase (iNOS) and IL-6 mRNA levels. In the ALI model, CJT decreased the inflammatory cell count in the bronchoalveolar lavage fluid (BALF) while IL-6 levels were reduced in CJT-treated mice compared with the ALI control mice. CJT also inhibited airway inflammation by reducing iNOS expression in lung tissue. In conclusion, our results indicate that CJT inhibits inflammatory responses in LPS-stimulated RAW264.7 cells and in the LPS-induced ALI model. Therefore, we suggest that CJT has the potential to treat inflammatory diseases such as pneumonia.

Melatonin attenuates neutrophil inflammation and mucus secretion in cigarette smoke-induced chronic obstructive pulmonary diseases via the suppression of Erk-Sp1 signaling.

The incidence of chronic obstructive pulmonary disease (COPD) has substantially increased in recent decade. Cigarette smoke (CS) is the most important risk factor in the development of COPD. In this study, we investigated the effects of melatonin on the development of COPD using a CS and lipopolysaccharide (LPS)-induced COPD model and cigarette smoke condensate (CSC)-stimulated NCI-H292 cells, a human mucoepidermoid carcinoma cell. On day 4, the mice were treated intranasally with LPS. The mice were exposed to CS for 1 hr per day (8 cigarettes per day) from day 1 to day 7. Melatonin (10 or 20 mg/kg) was injected intraperitoneally 1 hr before CS exposure. Melatonin markedly decreased the neutrophil count in the BALF, with reduction in the proinflammatory mediators and MUC5AC. Melatonin inhibited Erk phosphorylation and Sp1 expression induced by CS and LPS treatment. Additionally, melatonin decreased airway inflammation with a reduction in myeloperoxidase expression in lung tissue. In in vitro experiments, melatonin suppressed the elevated expression of proinflammatory mediators induced by CSC treatment. Melatonin reduced Erk phosphorylation and Sp1 expression in CSC-stimulated H292 cells. In addition, cotreatment of melatonin and Erk inhibitors significantly limited the proinflammatory mediators with greater reductions in Erk phosphorylation and Sp1 expression than that observed in H292 cells treated with Erk inhibitor alone. Taken together, melatonin effectively inhibited the neutrophil airway inflammation induced by CS and LPS treatment, which was closely related to downregulation of Erk phosphorylation. These findings suggest that melatonin has a therapeutic potential for the treatment of COPD.

Anti-inflammatory activities of Physalis alkekengi var. franchetii extract through the inhibition of MMP-9 and AP-1 activation.

Physalis alkekengi has been traditionally used for the treatment of coughs, middle ear infections, and sore throats in Korea, Europe, and China. It exhibits a variety of pharmacological activities such as anti-inflammatory, anti-oxidant, and anti-cancer effects. The anti-inflammatory effects of the P. alkekengi methanol extract (PA) and its molecular mechanisms have not yet been fully investigated. In the present study, the chromatogram of PA was established by UPLC analysis. The anti-inflammatory effects of PA were also investigated using murine microphage cell lines, RAW 264.7 cells, and a murine model of OVA induced asthma. In LPS-stimulated RAW264.7 cells, PA reduced the MMP-9 expression with decreases in the production of nitric oxide, inteleukin-6, and tumor necrosis factor-α. Furthermore, PA suppressed the phosphorylation of MAPKs, which resulted in the inhibition of AP-1 activation. These effects of PA were consistent with the results of the in vivo experiment. PA-treated mice significantly inhibited inflammatory cell counts and cytokine production in bronchoalveolar lavage fluids and airway-hyperresponsiveness in OVA-induced asthmatic mice. PA treated mice also showed a marked inhibition of inducible nitric oxide synthase and MMP-9 expression. In conclusion, our results suggest that PA may be a valuable therapeutic material in treating various inflammatory diseases, including allergic asthma.

Melatonin reduces airway inflammation in ovalbumin-induced asthma.

Asthma is a common chronic inflammatory airway disease that is recognized as a major public health problem. In this study, we evaluated the effects of melatonin on allergic asthma using a murine model of ovalbumin (OVA)-induced allergic asthma and BEAS-2B cells. To induce allergic asthma, the mice were sensitized and airway-challenged with OVA. Melatonin was administered by intraperitoneal injection once per day at doses of 10 and 15 mg/kg from days 21 to 23 after the initial OVA sensitization. We investigated the effects of melatonin on proinflammatory cytokines and matrix metalloproteinase-9 (MMP-9) activity and expression in tumor necrosis factor (TNF)-α-stimulated BEAS-2B cells. The administration of melatonin significantly decreased the number of inflammatory cells, airway hyperresponsiveness, and immunoglobulin (Ig) E with reductions in interleukin (IL)-4, IL-5, and IL-13. Melatonin attenuated the airway inflammation and the mucus production in lung tissue and significantly suppressed elevated MMP-9 expression and activity induced by an OVA challenge. In TNF-α-stimulated BEAS-2B cells, treatment with melatonin significantly reduced the levels of proinflammatory cytokines and lowered the expression and activity of MMP-9. These results indicate that melatonin effectively suppressed allergic asthma induced by an OVA challenge. The results suggest a potential role for melatonin in treating asthma.

Siegesbeckia glabrescens attenuates allergic airway inflammation in LPS-stimulated RAW 264.7 cells and OVA induced asthma murine model.

Siegesbeckia glabrescens (SG) is a plant growing in Korea that is used as a traditional medicine for various inflammatory diseases. In this study, we investigated the protective effects of SG extract on allergic asthma in an ovalbumin (OVA)-induced asthma murine model and lipopolysaccharide (LPS)-stimulated RAW264.7 cells. Female BALB/c mice were sensitized by intraperitoneal injection of OVA on days 0 and 14 and then challenged with OVA from days 21 to 23. SG (30mg/kg) was administered by oral gavage 1h before the OVA challenge. LPS-stimulated RAW264.7 cells were evaluated to determine their levels of nitric oxide (NO). The SG significantly reduced the number of inflammatory cells in bronchoalveolar lavage (BAL) fluid and also reduced IL-4, IL-5, IL-13, eotaxin and immunoglobulin E in OVA-sensitized/challenged mice. SG also effectively reduced airway inflammation and mucus overproduction in lung tissue in addition to decreasing the expression of iNOS and COX-2. In LPS-stimulated RAW264.7 cells, SG treatment significantly reduced the levels of NO. These findings indicate that SG effectively suppressed inflammatory responses, and its effects appear to be related to reduction in iNOS and COX-2 expression. Therefore, we suggest that SG may have potential use as a therapeutic agent for inflammatory diseases such as allergic asthma.

Inhibitory effects of Picrasma quassioides (D.Don) Benn. on airway inflammation in a murine model of allergic asthma.

Picrasma quassioides (D.Don) Benn. (PQ) is used in traditional medicine for the treatment of inflammatory conditions, including gastritis. This study aimed to evaluate the inhibitory effects of PQ on the inflammatory responses in mice with allergic asthma induced by ovalbumin (OVA) and in lipopolysaccharide (LPS)­stimulated RAW264.7 cells. To induce allergic asthma, the mice underwent OVA sensitization on days 0 and 14 and then were challenged with OVA from days 21­23. The mice were administered 15 and 30 mg/kg doses of PQ 1 h prior to the OVA challenge. The PQ treatment decreased the inflammatory cell count in the bronchoalveolar lavage fluid of the mice and reduced the levels of interleukin (IL)­4, IL­5, IL­13 and immunoglobulin (Ig)E when compared with those in the OVA group. The PQ treatment also reduced the airway hyperresponsiveness induced by the OVA challenge, attenuated the recruitment of inflammatory cells and the mucus production in the airways of the mice. In the LPS­stimulated RAW264.7 cells, the PQ treatment reduced the overexpression of inducible nitric oxide synthase (iNOS). The results indicated that PQ inhibits inflammatory responses in mice with OVA­sensitized/challenged allergic asthma and in LPS­stimulated RAW264.7 cells. These effects were considered to be associated with the suppression of iNOS expression. Therefore, PQ may have the potential to treat airway inflammatory diseases, including allergic asthma.

Melatonin inhibits MUC5AC production via suppression of MAPK signaling in human airway epithelial cells.

Mucus acts as a primary defense system in the airway against various stimuli. However, excess mucus production causes a reduction in lung function via limitation of the airflow in the airway of patients suffering from asthma or chronic obstructive pulmonary disease (COPD). In this study, we evaluated the effects of melatonin on the production of MUC5AC, a major constituent of the mucin that is secreted from the airway, using epidermal growth factor (EGF)-stimulated NCI-H292 cells, a human mucoepidermoid carcinoma cell line, and an ovalbumin (OVA)-induced asthma murine model. Melatonin treatment significantly reduced the mRNA and protein levels of MUC5AC and reduced interleukin (IL)-6 production in EGF-stimulated H292 cells. Melatonin markedly decreased the phosphorylation of MAPKs, including ERK1/2, JNK, and p-38, induced by EGF stimulation. These findings were consistent with the results using MAPK inhibitors. Particularly, co-treatment with melatonin and a MAPK inhibitor more effectively suppressed MAPK phosphorylation than treatment with a MAPK inhibitor alone, which resulted in a reduction in MUC5AC expression. In the asthma murine model, melatonin-treated mice exhibited a marked reduction in MUC5AC expression in the airway compared with the OVA-induced mice. These reductions were accompanied by reductions in proinflammatory cytokine production and inflammatory cell infiltration. Collectively, these findings indicate that melatonin effectively inhibits MUC5AC expression. These effects may be closely associated with the inhibition of MAPK phosphorylation. Furthermore, our study suggests that melatonin could represent a potential therapeutic for chronic airway diseases, such as asthma and COPD.

Homoegonol attenuates the asthmatic responses induced by ovalbumin challenge.

Homoegonol is a lignan derived from styraxlignolide A, which was isolated from Styrax japonica, a medicinal plant widely used for treatment of inflammatory diseases in Korea. We investigated the efficacy of homoegonol for the treatment of allergic asthma using an ovalbumin (OVA)-induced murine asthma model. The mice were sensitized through intraperitoneal injections of OVA on days 0 and 14. On days 21, 22 and 23 after the initial OVA sensitization, the mice were received OVA airway challenge. Homoegonol was administered by oral gavage at a dose of 30 mg/kg 1 h prior to the OVA challenge. The homoegonol-treated mice exhibited reduced inflammatory cell counts and Th2 cytokines in BALF, AHR, and IgE in the serum compared with the OVA-sensitized/challenged mice. The histological analysis of the lung tissue revealed that the administration of homoegonol attenuated the airway inflammation and the mucus overproduction in airway epithelial lesions induced by OVA through a reduction in expression of inducible nitric oxide synthase and matrix metalloproteinase-9. These findings indicate that homoegonol effectively suppresses the asthmatic responses induced by OVA challenge and suggests that homoegonol exhibits potential as therapeutic drug for allergic asthma.

EC-18, a synthetic monoacetyldiglyceride (1-palmitoyl-2-linoleoyl-3-acetylglycerol), attenuates the asthmatic response in an aluminum hydroxide/ovalbumin-induced model of asthma.

EC-18 is a synthetic monoacetyldiaglyceride that is a major constituent in antlers of Sika deer (Cervus nippon Temmenick). In this study, we evaluated the protective effects of EC-18 on Th2-type cytokines, eosinophil infiltration, and other factors in an aluminum hydroxide/ovalbumin (OVA)-induced murine asthma model. Mice were sensitized on days 0 and 14 by intraperitoneal injection of OVA with aluminum hydroxide. On days 21, 22 and 23 after the initial sensitization, the mice received an airway challenge with OVA for 1h using an ultrasonic nebulizer. EC-18 was administered to mice by oral gavage at doses of 30mg/kg and 60mg/kg once daily from day 18 to 23. Methacholine responsiveness was measured 24h after the final OVA challenge, and the bronchoalveolar lavage fluid (BALF) was collected 48h after the final OVA challenge. EC-18 significantly reduced methacholine responsiveness, T helper type 2 (Th2) cytokines, eotaxin-1, immunoglobulin (Ig) E, IgG, and the number of inflammatory cells. In addition, EC-18-treated mice exhibited the reduction in the expression of inducible nitric oxide synthase (iNOS) in lung tissue. In the histological analysis using hematoxylin-eosin stain and periodic acid-Schiff stain, EC-18 attenuated the infiltration of inflammatory cells into the airway and reduced the level of mucus production. Our results showed that EC-18 effectively suppressed the asthmatic response induced by OVA challenge. These effects were considered to be associated with iNOS suppression. In conclusion, this study suggests that EC-18 may be a therapeutic agent for allergic asthma.

Inhibitory effects of Pycnogenol® (French maritime pine bark extract) on airway inflammation in ovalbumin-induced allergic asthma.

Pycnogenol® (PYC) is a standardized extracts from the bark of the French maritime pine (Pinus maritime) and used as a herbal remedy for various diseases. In this study, we evaluated the effects of PYC on airway inflammation using a model of ovalbumin (OVA)-induced allergic asthma and RAW264.7 cells. PYC decreased nitric oxide production and reduced the interleukine (IL)-1ß and IL-6 levels in LPS-stimulated RAW264.7 cells. PYC also reduced the expression of inducible nitric oxide synthase (iNOS) and matrix metalloproteinase (MMP)-9 and enhanced the expression of hemeoxygenase (HO)-1. In the in vivo experiment, PYC decreased the inflammatory cell count and the levels of IL-4, IL-5, IL-13, and immunoglobulin (Ig) E in BALF or serum. These results are consistent with the histological analysis findings, which showed that PYC attenuated the airway inflammation and mucus hypersecretion induced by OVA challenge. In addition, PYC enhanced the expression of HO-1. In contrast, PYC inhibited the elevated expression of iNOS and MMP-9 proteins induced by OVA challenge. In conclusion, PYC exhibits protective effects against OVA-induced asthma and LPS-stimulated RAW264.7 cells. These results suggest that PYC has potential as a therapeutic agent for the treatment of allergic asthma.

Diallyl-disulfide, an organosulfur compound of garlic, attenuates airway inflammation via activation of the Nrf-2/HO-1 pathway and NF-kappaB suppression.

Diallyl disulfide (DADS) is a major organosulfur compound found in garlic oil that is widely used as a flavoring agent. In this study, we evaluated the effects of DADS on airway inflammation using an ovalbumin-induced model of allergic asthma and RAW264.7 cells. DADS decreased nitric oxide production with a reduction in the levels of interleukins (IL)-1ß and IL-6 in RAW264.7 cells stimulated with LPS. DADS also reduced the expression of proinflammatory proteins including inducible nitric oxide synthase (iNOS), nuclear factor (NF)-κB, and matrix metalloproteinase (MMP)-9, and it enhanced the expression of antioxidant proteins including Nrf-2 and hemeoxygenase (HO)-1. In in vivo experiments, DADS decreased the inflammatory cell count in the bronchoalveolar lavage fluid (BALF) with IL-4, IL-5, IL-13, and immunoglobulin (Ig) E. These results were consistent with the histological analysis. DADS attenuated the airway inflammation and mucus hypersecretion induced by OVA challenge. In addition, DADS induced the activation of Nrf-2 and the expression of HO-1. In contrast, DADS reduced the activation of NF-κB, iNOS and MMP-9. In conclusion, DADS reduced the airway inflammation via regulation of Nrf-2/HO-1 and NF-κB. These results suggest that DADS might represent a useful new oral therapy to treat allergic asthma.