montelukast and Airway-Remodeling

Asthma is a chronic inflammatory and allergic disease that is mainly characterized by reversible airway obstruction and bronchial hyperresponsiveness. The incidence of asthma is increasing with more than 350 million people worldwide are affected. Up to now, there is no therapeutic option for asthma and most of the prescribed drugs aim to ameliorate the symptoms of the disease especially during the acute exacerbations after trigger exposure. Asthma is a heterogonous disease that involves interactions between inflammatory mediators and cellular components within the disease microenvironment including inflammatory and structural cells. Cysteinyl leukotrienes (cys-LTs) are inflammatory lipid mediators that have potent roles in asthma pathogenesis. CysLTs consisting of LTC

Topics: Acetates; Airway Remodeling; Animals; Anti-Asthmatic Agents; Asthma; Bronchial Hyperreactivity; Cyclopropanes; Cysteine; Gene Expression; Humans; Hypersensitivity; Indoles; Inflammation Mediators; Leukotriene Antagonists; Leukotriene D4; Leukotrienes; Phenylcarbamates; Quinolines; Receptors, Leukotriene; Sulfides; Sulfonamides; Tosyl Compounds

Anti-inflammatory preventive treatment is recommended in cases of persistent asthma. Besides inhaled corticosteroids (ICS), which represent the mainstay of treatment, other therapeutic options are available, of which only antileukotrienes are approved for all age groups.. Given as a substitute of low-dose ICS, montelukast prevents exacerbations as efficiently and for a longer period than long-acting β2-agonists. Montelukast is as efficient as doubling the dose of ICS on asthma symptoms in cases of inadequate control with low-dose ICS. Combined with ICS, it can lead to better control of asthma and potentially to ICS sparing.. Given the efficacy, tolerance and long-term treatment compliance of montelukast in mild persistent asthma in adults and children, montelukast, given as a substitute or combined with ICS, could contribute to enhanced control of asthma, especially in children.

Topics: Acetates; Adrenal Cortex Hormones; Adult; Airway Remodeling; Anti-Asthmatic Agents; Asthma; Bronchodilator Agents; Child; Cyclopropanes; Cytokines; Drug Therapy, Combination; France; Humans; Inflammation; Leukotriene Antagonists; Leukotrienes; Models, Biological; Practice Guidelines as Topic; Prevalence; Quinolines; Randomized Controlled Trials as Topic; Receptors, Leukotriene; Sulfides

Evidence has demonstrated that the distal lung, which includes airways of < 2 mm in diameter and lung parenchyma, constitutes an important component of asthma pathology. Cysteinyl leukotrienes (CysLTs) are potent proinflammatory mediators and bronchoconstrictors involved in the asthmatic process. Guidelines recommend the leukotriene-modifying agents for asthma treatment. We hypothesized that a leukotriene receptor antagonist with an inhaled corticosteroid (ICS) and long-acting β2 agonist (LABA) combination would improve small airways function in moderate-to- severe asthmatics evaluated by physiological tests and high-resolution computed tomography (HRCT) analysis. This study was performed at a tertiary university hospital in Beijing.. This was a randomized, double-blind, parallel study performed in 38 patients with moderate-to-severe asthma treated with salmeterol/futicasone (SFC) plus montelukast (SFC+M) or SFC plus placebo over 24 weeks. Small airway function was assessed by physiological studies and HRCT image analysis.. Montelukast significantly improved air trapping as expressed by the residual volume (RV)/total lung capacity (TLC). Over 24 weeks of treatment, RV/TLC was improved by (15.41 ± 6.67)% in patients receiving SFC+M while RV/TLC was decreased by (8.57 ± 10.26)% in patients receiving SFC alone, the difference between the two groups was significant (P = 0.02). There was a trend towards a significant difference in forced expiratory volume in the first second (FEV1)/forced vital capacity (FVC) in the SFC+M group compared to that in the SFC group ((17.87 ± 8.17)% vs. (12.28 ± 9.20)%, P = 0.056). There was no significant change in percentage wall area (WA%) after 24 weeks of add-on treatment with montelukast. Patients receiving SFC+M showed significant improvement in the ratio of CT-determined values at full expiration to those at full inspiration (E/I ratio) (0.894 ± 0.005 vs. 0.871 ± 0.003, P = 0.002).. We have shown, using lung function tests and HRCT image technique, that add-on therapy with montelukast improves distal lung function reflected by air trapping, but not airway wall thickness in moderate-to-severe asthma.

Topics: Acetates; Adult; Airway Remodeling; Anti-Asthmatic Agents; Asthma; Cyclopropanes; Double-Blind Method; Female; Forced Expiratory Volume; Humans; Leukotriene Antagonists; Male; Middle Aged; Pilot Projects; Quinolines; Sulfides; Total Lung Capacity

Vitamin D is commonly known for its properties of airway remodeling inhibition. Due to this, we decided to analyze the action of calcitriol with anti-asthmatic drugs in airway remodeling. The HFL1 cell line was treated with calcitriol, beclomethasone 17-propionate, montelukast sodium, LTD4 and TGF-β in different combinations. Real-time PCR was used to analyzed the expression of ACTA2, CDH-1, Vimentin, ADAM33, MMP-9 and CysLTR1 on the mRNA level, whereas Western blot was used to analyze gene expression on the protein level. One-way analysis variants, the Kruskal-Wallis test, Student's

Topics: ADAM Proteins; Airway Remodeling; Anti-Asthmatic Agents; Calcitriol; Humans; Leukotriene D4; Transforming Growth Factor beta; Vimentin; Vitamin D; Vitamins

It is well known that the prevalence of asthma is higher in athletes, including Olympic athletes, than in the general population. In this study, we analyzed the mechanism of exercise-induced bronchoconstriction by using animal models of athlete asthma. Mice were made to exercise on a treadmill for a total duration of 1 week, 3 weeks, or 5 weeks. We analyzed airway responsiveness, BAL fluid, lung homogenates, and tissue histology for each period. In mice that were treated (i.e., the treatment model), treatments were administered from the fourth to the fifth week. We also collected induced sputum from human athletes with asthma and analyzed the supernatants. Airway responsiveness to methacholine was enhanced with repeated exercise stimulation, although the cell composition in BAL fluid did not change. Exercise induced hypertrophy of airway smooth muscle and subepithelial collagen deposition. Cysteinyl-leukotriene (Cys-LT) levels were significantly increased with exercise duration. Montelukast treatment significantly reduced airway hyperresponsiveness (AHR) and airway remodeling. Expression of PLA

Topics: Acetates; Airway Remodeling; Animals; Asthma; Bronchial Hyperreactivity; Bronchoconstriction; Cyclopropanes; Cysteine; Female; Group II Phospholipases A2; Leukotrienes; Lung; Methacholine Chloride; Mice; Mice, Inbred BALB C; Physical Conditioning, Animal; Quinolines; Respiratory Hypersensitivity; Sulfides

Asthma is characterized by airway hyperresponsiveness (AHR) and inflammation leading to airway remodeling (AR). In children, AR may occur very early prior to the age of 6 years. Treatments to prevent or reverse AR are unknown.. We sought to determine (i) whether short allergenic sensitization at a young age in a mouse model may induce enhanced AR and inflammation compared to adults; (ii) the effect of Montelukast on such AR.. Immature and adult Balb/c mice were sensitized and challenged with ovalbumin. AHR and AR were measured using cultured precision-cut lung slices and inflammation by bronchoalveolar lavage. Experiments were repeated after administration of Montelukast.. OVA-challenged mice developed AHR to methacholine regardless of age of first exposure to OVA. Young mice developed greater thickened basement membrane, increased smooth muscle mass, and increased area of bronchovascular fibrosis compared with adult mice. Cellular infiltrates in BAL differed depending upon animal age at first exposure with higher eosinophilia measured in younger animals. Montelukast decreased ASM mass, BAL cellularity.. We provide thus evidence for a greater degree of AR after allergenic sensitization and challenge in younger mice versus adults. This study provides proof of concept that airway remodeling can be prevented and reversed in this case by anti-asthmatic drug Montelukast in this model.

Topics: Acetates; Age Factors; Airway Remodeling; Allergens; Animals; Anti-Asthmatic Agents; Asthma; Bronchoalveolar Lavage Fluid; Cyclopropanes; Disease Models, Animal; Female; Lung; Mice, Inbred BALB C; Ovalbumin; Quinolines; Sulfides

To study the effect of montelukast sodium (MK), a leukotriene receptor antagonist, and bacterial lysates (OM-85BV), used alone or in combination, on airway remodeling and the expression of transforming growth factor-β1 (TGF-β1) and Smad7 in guinea pigs with bronchial asthma and their correlation.. A total of 40 male Hartley guinea pigs were randomly divided into normal control group, asthma group, MK group, OM-85BV group, and MK+OM-85BV group, with 8 guinea pigs in each group. Intraperitoneal injection of 10% ovalbumin (OVA) for sensitization and aerosol inhalation of 1% OVA for challenge were performed to establish a model of airway remodeling of asthma in all of the groups apart from the normal control group, which were treated with normal saline. In the stage of challenge by aerosol inhalation, the guinea pigs in the MK, OM-85BV, and MK+OM-85BV groups were given corresponding suspension by gavage, and those in the normal control and asthma groups were given an equal volume of normal saline by gavage. Bronchoalveolar lavage fluid (BALF) of the guinea pigs was collected within 24 hours after challenge, and ELISA was used to measure the levels of TGF-β1 and Smad7 in BALF. The guinea pigs were sacrificed and the pathological section of lung tissue was prepared to observe the degree of airway remodeling. An image analysis technique was used to measure perimeter of the basement membrane (Pbm), total bronchial wall area (Wat), and airway bronchial smooth muscle area (Wam). Pearson linear regression was used to investigate the correlation between two variables.. According to the lung pathological section, compared with the normal control group, the asthma, MK, OM-85BV, and MK+OM-85BV groups had significant thickening of bronchial smooth muscle and alveolar wall, significantly higher Wat/Pbm and Wam/Pbm, a significantly higher level of TGF-β1, and a significantly lower level of Smad7 (P<0.05). Compared with the asthma group, the MK, OM-85BV, and MK+OM-85BV groups had a significant improvement in pathological injury, significantly lower Wat/Pbm and Wam/Pbm, a significantly lower level of TGF-β1, and a significantly higher level of Smad7 (P<0.05). The MK+OM-85BV group had significantly greater improvements than the MK group and the OM-85BV group (P<0.05). The expression of TGF-β1 was negatively correlated with that of Smad7 and positively correlated with Wat/Pbm and Wam/Pbm, and the expression of Smad7 was negatively correlated with Wat/Pbm and Wam/Pbm (P<0.01).. MK and OM-85BV, used alone or in combination, can reduce airway remodeling in guinea pigs with asthma, and MK combined with OM-85BV has the best effect, possibly by reducing TGF-β1 expression, increasing Smad7 expression, and improving the TGF-β1/Smad7 imbalance.

Topics: Acetates; Airway Remodeling; Animals; Asthma; Cell Extracts; Cyclopropanes; Guinea Pigs; Lung; Male; Ovalbumin; Quinolines; Sulfides; Transforming Growth Factor beta1

Asthma is a pathology characterized by chronic inflammation and remodeling of the airways.. To evaluate the effect of montelukast treatment on markers of airway inflammation and remodeling in children with mild asthma and to evaluate if the administration of montelukast to children with mild asthma could inhibit the release of matrix metallopeptidase 9, matrix metallopeptidase 12, tissue inhibitor of metalloproteinase 1, transforming growth factor beta 1, C-peptide terminal procollagen type (PICP), and eosinophils count, which are markers of inflammation and remodeling in induced sputum.. Thirty children with mild asthma were recruited. They were randomized into two groups: group A received montelukast and as needed beta-2-agonist for 8 weeks (T0-T1), whereas group B received placebo and as needed beta-2-agonist for 8 weeks. After 2 weeks of washout (T1-T2), they were reallocated for treatment according a crossover design (T2-T3). Tests for lung function, oral exhaled nitric oxide, and hypertonic saline solution-induced sputum level were performed at T0-T1-T2-T3.. In the placebo group, the PICP mean (standard deviation [SD]) value at baseline was 2279.42 ± 2530.77 pg/mL and 1916.00 ± 2178.75 pg/mL after treatment. Patients treated with montelukast, in contrast, showed a baseline mean (SD) value of 2439.29 ± 2834.51 pg/mL and 1406.72 ± 1508.65 pg/mL after treatment. The difference between the mean pre- and posttreatment decrease of PICP in the two groups was statistically significant (delta -690.21 pg/mL [95% confidence interval, -1220.83 to -159.5844 pg/mL]; p = 0.011). The mean (SD) percentage of the eosinophil count in the placebo group was 3.11 ± 4.03% at baseline and 4.86 ± 5.83% after treatment. Patients treated with montelukast, in contrast, showed a percentage mean (SD) value at baseline of 4.51 ± 5.48% and, after treatment, of 3.06 ± 3.29%. The difference between the mean pre- and posttreatment decrease of the percentage eosinophil count in the two groups was statistically significant (delta -2.76% [95% confidence interval, -4.65 to -0.87%]; p = 0.004).. This study investigated in vivo effects of montelukast on remodeling markers. The reduction of PICP levels and eosinophil count supported the hypothesis that montelukast can modulate collagen deposition in airways and reduce eosinophilic airway inflammation. Clinical Trials database clinicaltrials.gov (NCT00875082).

Topics: Acetates; Adolescent; Airway Remodeling; Anti-Asthmatic Agents; Asthma; Biomarkers; Child; Cyclopropanes; Female; Humans; Male; Quinolines; Respiratory Function Tests; Sulfides; Treatment Outcome

To study the dynamic changes in the percentage of Th17 cells/CD4. Balb/c mice were randomly divided into blank group, asthma group, and montelukast sodium group. The asthmatic mouse model of airway remodeling was established by sensitization with intraperitoneal injection of chicken ovalbumin (OVA) and aluminum hydroxide suspension and aerosol inhalation of OVA. The mice in the blank group were given normal saline, and those in the montelukast sodium group were given montelukast sodium by gavage before aerosol inhalation. Eight mice were randomly sacrificed within 24 hours after 2, 4, and 8 weeks of aerosol inhalation. The pathological sections of lung tissue were used to observe the degree of airway remodeling. Flow cytometry was used to measure the percentages of Th17 cells and CD4. The asthma group and the montelukast sodium group had significantly higher bronchial wall thickness and smooth muscle thickness at all time points compared with the blank group (P<0.05). At 8 weeks of intervention, the montelukast sodium group had significantly greater improvements in the above changes compared with the asthma group (P<0.05). Compared with the blank group, the asthma group and the montelukast sodium group had significant increases in Th17 cells (positively correlated with airway remodeling) and significant reductions in CD4. Montelukast sodium intervention can alleviate airway remodeling and achieve better improvements over the time of intervention. The possible mechanism may be related to the improvement of immunologic derangement of CD4

Topics: Acetates; Airway Remodeling; Animals; Asthma; Cyclopropanes; Female; Lung; Mice; Mice, Inbred BALB C; Quinolines; Sulfides; T-Lymphocytes, Regulatory; Th17 Cells

Epithelial to mesenchymal transition (EMT) is a mechanism by which eosinophils can induce airway remodeling. Montelukast, an antagonist of the cysteinyl leukotriene receptor, can suppress airway remodeling in asthma. The purpose of this study was to evaluate whether montelukast can ameliorate airway remodeling by blocking EMT induced by eosinophils. EMT induced was assessed using a co-culture system of human bronchial epithelial cells and human eosinophils or the eosinophilic leukemia cell lines, Eol-1. Montelukast inhibited co-culture associated morphological changes of BEAS-2b cells, decreased the expression of vimentin and collagen I, and increased the expression of E-cadherin. Montelukast mitigated the rise of TGF-β1 production and Smad3 phosphorylation. Co-culture of human eosinophils with BEAS-2B cells significantly enhanced the production of CysLTs compared with BEAS-2B cells or eosinophils alone. The increase of CysLTs was abolished by montelukast pre-treatment. Montelukast had similar effects when co-culture system of Eol-1 and BEAS-2B was used. This study showed that montelukast suppresses eosinophils-induced EMT of airway epithelial cells. This finding may explain the mechanism of montelukast-mediated amelioration of airway remodeling in bronchial asthma.

Topics: Acetates; Airway Remodeling; Asthma; Bronchi; Cell Line, Tumor; Coculture Techniques; Collagen Type I; Cyclopropanes; Cysteine; Eosinophils; Epithelial-Mesenchymal Transition; Humans; Leukotriene Antagonists; Leukotrienes; Phosphorylation; Quinolines; Respiratory Mucosa; Smad3 Protein; Sulfides; Transforming Growth Factor beta1; Vimentin

To investigate the effect of montelukast on the expression of sensory neuropeptide (neurokinin-1) receptor (NK1R) in young asthmatic rats with airway remodeling.. Twenty-four Sprague-Dawley rats were randomly divided into control group (n=8), asthma (n=8), and montelukast groups (n=8). A rat model of asthma was induced by ovalbumin (OVA) inhalation. Normal saline was used instead of sensitizing solution and 1% OVA in the control group. Each rat in the montelukast group was given montelukast (15 mg/kg) by gavage 2 h before OVA inhalation. All rats received their respective treatments for 8 weeks. Immunohistochemistry, real-time PCR and Western blot were used to measure the mRNA and protein expression levels of NK1R in asthmatic airway remolding and to evaluate the effect of montelukast on NK1R expression.. The asthma group showed significantly higher mRNA and protein expression levels of NK1R than the control group (P<0.01). The mRNA and protein expression levels of NK1R in the montelukast group were significantly lower than in the asthma group (P<0.05), but significantly higher than in the control group (P<0.01).. Rats with induced asthma have upregulated NK1R expression in the airway, and montelukast can downregulate NK1R expression during airway remodeling.

Topics: Acetates; Airway Remodeling; Animals; Anti-Asthmatic Agents; Asthma; Cyclopropanes; Female; Leukotriene Antagonists; Quinolines; Rats; Rats, Sprague-Dawley; Receptors, Neurokinin-1; RNA, Messenger; Sulfides

This study examined the effect of montelukast and beclomethasone on airway remodeling in murine model of asthma. Mice were sensitized by i.p. injection of ovalbumin (OVA) on days 0 and 14, and then challenged by nebulization of 1% OVA 3 days/week for 6 or 10 weeks. Results of 6-week OVA-challenged group showed moderate inflammation, but the 10-week OVA-challenged group exhibited mild inflammation. The OVA challenge (6 and 10 weeks) exhibited marked airway fibrosis, illustrated by significant increase in goblet cell hyperplasia and epithelial thickness, increased lung content of collagen and transforming growth factor-β(1), together with a decrease in nitric oxide production; also, there was an increase in bronchoalveolar lavage fluid level of interleukin-13. Administration of montelukast or beclomethasone before each OVA challenge was capable of restoring most of the measured parameters to near normal levels. Inhalation of beclomethasone has a similar role in airway remodeling as montelukast, but its effects in regulating inflammatory changes is less pronounced than montelukast.

Topics: Acetates; Administration, Inhalation; Airway Remodeling; Animals; Anti-Asthmatic Agents; Asthma; Beclomethasone; Cyclopropanes; Disease Models, Animal; Inflammation; Male; Mice; Ovalbumin; Quinolines; Severity of Illness Index; Sulfides; Time Factors

Airway remodeling in bronchial asthma results from chronic, persistent airway inflammation. The effects of the reversal of airway remodeling by drug interventions remain to be elucidated. We investigated the effects of ONO-1301, a novel prostacyclin agonist with thromboxane inhibitory activity, on the prevention and reversibility of airway remodeling in an experimental chronic asthma model. Mice sensitized and challenged to ovalbumin (OVA) three times a week for 5 consecutive weeks were administered ONO-1301 or vehicle twice a day from the fourth week of OVA challenges. Twenty-four hours after the final OVA challenge, airway hyperresponsiveness (AHR) was assessed, and bronchoalveolar lavage was performed. Lung specimens were excised for staining to detect goblet-cell metaplasia, airway smooth muscle, and submucosal fibrosis. Mice administered ONO-1301 showed limited increases in AHR compared with mice administered the vehicle. The histological findings of airway remodeling were improved in ONO-1301-treated mice compared with vehicle-treated mice. Presumably, these therapeutic effects of ONO-1301 are attributable to the up-regulation of production of hepatocyte growth factor (HGF) in lung tissue, because the neutralization of HGF by antibodies prevented the effects of ONO-1301 on AHR and airway remodeling. Mice administered ONO-1301 showed similar levels of AHR and airway remodeling as mice administered montelukast, a cysteinyl-leukotriene-1 receptor antagonist, and lower levels were observed in mice administered dexamethasone. These data suggest that ONO-1301 exerts the effect of reversing airway remodeling, at least in part through an elevation of HGF in the lungs, and may be effective as an anti-remodeling drug in the treatment of asthma.

Topics: Acetates; Airway Remodeling; Animals; Asthma; Bronchial Hyperreactivity; Bronchoalveolar Lavage Fluid; Cyclopropanes; Dexamethasone; Epoprostenol; Female; Goblet Cells; Hepatocyte Growth Factor; Inflammation; Lung; Metaplasia; Mice; Mice, Inbred BALB C; Muscle, Smooth; Ovalbumin; Pulmonary Fibrosis; Pyridines; Quinolines; Receptors, Leukotriene; Sulfides; Thromboxanes; Up-Regulation

We demonstrated previously that GATA-3 overexpression markedly enhanced allergen-induced airway inflammation and airway remodelling, including subepithelial fibrosis, and smooth muscle cell hyperplasia, in transgenic mice.. Because cysteinyl leukotrienes (cysLTs) have been shown to be involved in such structural changes, the effects of a specific cysLT1 receptor antagonist, montelukast, were evaluated in a mouse model of chronic asthma.. GATA-3-overexpressing mice and wild-type Balb/c mice were sensitized and repeatedly challenged by ovalbumin (OVA) or saline. The effects of montelukast on the development of airway remodelling were compared between the two mouse genotypes.. CysLTs in the lung were increased after repeated allergen challenges, and significantly enhanced in GATA-3-overexpressing mice. The enhanced cysLT levels were accompanied by the development of eosinophilia, smooth muscle cell hyperplasia, and increased stromal cell-derived factor-1 gene expression with a small increase in pro-collagen gene expression in OVA-challenged GATA-3-overexpressing mice, but not in wild-type mice. Montelukast significantly decreased lung cysLT levels and inhibited the GATA-3-overexpression-related airway remodelling, potently preventing smooth muscle cell hyperplasia, but partially suppressed the increased pro-collagen gene expression and eosinophilic inflammation. Increases in the levels of IL-4, IL-5, IL-13, and eotaxin in bronchial lavage and TGF-β gene expression in the lungs were induced by OVA in both mouse genotypes. Montelukast treatment also significantly reduced these levels to the levels seen after saline challenges in GATA-3-overexpressing mice.. Montelukast efficaciously prevented airway inflammation and remodelling in a GATA-3-overexpression antigen challenge mouse model by decreasing the cysLT-driven Th2 cytokine cycle of amplification of airway pathologies.

Topics: Acetates; Airway Remodeling; Animals; Cyclopropanes; Disease Models, Animal; GATA3 Transcription Factor; Mice; Mice, Inbred BALB C; Mice, Transgenic; Quinolines; Receptors, Leukotriene; Reverse Transcriptase Polymerase Chain Reaction; Sulfides; Th2 Cells

To investigate the effect of montelukast (MK) on airway inflammation and remodeling in asthmatic rats, and to explore the regulating role of MK on vascular endothelial growth factor (VEGF) and its receptors.. Twenty-four male Sprague-Dawley rats were randomly divided into 3 groups, a control group (n = 8), an asthmatic group (n = 8) and a MK treated group (n = 8). The rats were sensitized with ovalbumin and AL (OH3), and repeatedly exposed to aerosolized ovalbumin. Airway reactivity of the animals were measured by animal lung function meter. VEGF levels and leukotriene D(4) (LTD(4)) in serum were measured by enzyme linked-immunosorbent assay (ELISA). The pathologic changes of bronchi and the lung tissue were evaluated, and the expression of VEGF and its acceptors was analyzed with immunohistochemistry. The vascular counts and vascular smooth muscle thickness were measured by using image analysis system.. The bronchial provocation test showed that, in the asthmatic group, the average expiratory resistance increased remarkably. The serum levels of VEGF and LTD(4) in the asthmatic group were 31 +/- 6 and 11 +/- 4 respectively, significantly higher than those in the control group (17 +/- 5 and 6.1 +/- 0.7) respectively and in the MK group (15 +/- 4 and 9.8 +/- 1.6) respectively. (F 63.78, 39.56 all P < 0.01). Immunohistochemistry showed that, the expression of VEGF, VEGFR(1) and VEGFR(2) in the asthmatic group were increased, as compared to those in the control group and the treated group. The vascular counts were 14 +/- 2, 22 +/- 2 and 16 +/- 4 in the control, the asthmatic, and the treated groups.. VEGF and its receptors were over-expressed in the sensitized rat model, and involved in angiogenesis and airway remodeling. MK may be effective in reducing allergic airway inflammation and airway remodeling through VEGF and VEGFR.

Topics: Acetates; Airway Remodeling; Animals; Asthma; Cyclopropanes; Leukotriene Antagonists; Leukotriene D4; Male; Neovascularization, Pathologic; Quinolines; Rats; Rats, Sprague-Dawley; Receptors, Vascular Endothelial Growth Factor; Sulfides; Vascular Endothelial Growth Factor A