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Efficacy of Salmeterol and Formoterol Combination Treatment in Mice with Chronic Obstructive Pulmonary Disease

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Efficacy of Salmeterol and Formoterol Combination Treatment in Mice with Chronic Obstructive Pulmonary Disease 1538 EXPERIMENTAL AND THERAPEUTIC MEDICINE 15: 1538-1545, 2018 Efficacy of salmeterol and formoterol combination treatment in mice with chronic obstructive pulmonary disease ZHIYUAN WANG, CHUNYAN WANG and XIAOLI YANG Department of Lung Disease, Yucheng City People's Hospital, Dezhou, Shangdong 350076, P.R. China Received April 8, 2016; Accepted March 23, 2017 DOI: 10.3892/etm.2017.5562 Abstract. Chronic obstructive pulmonary disease (COPD) impairment of activity, an increased risk of hospitalization and is a severe lung disease characterized by progressive airflow increased numerous symptoms including chronic bronchitis limitation. Salmeterol and formoterol are two commonly used and emphysema (5,6). In addition, a previous study reported drugs in COPD therapy, which act as β2-receptor agonists. In that ~80% of patients with COPD still exhibit deterioration the current study, a mouse model of COPD induced by airway of pulmonary function in a 3-year clinical investigation (7). lipopolysaccharide inhalation was established. The therapeutic Although the patients received different treatments, normal efficacy of salmeterol and formoterol co‑treatment was inves- pulmonary function deteriorated heterogeneously (7). tigated in this model over a 56-day-long observation period. It Salmeterol and formoterol are two commonly used drugs was also identified that functional residual capacity and inspi- in COPD therapy, which act as β2-receptor agonists (8). ratory resistance were significantly improved after salmeterol Salmeterol and formoterol were identified as β2-receptor and/or formoterol treatment compared with the control group agonists that inhibit early and late phase antigen-induced (all P<0.01). Furthermore, histological staining of lung tissue airway hyper‑responsiveness (9,10). Previous reports indicate samples indicated that inflammation, thickening of the smooth that the combination of inhaled salmeterol and formoterol muscle, goblet cell hyperplasia and pulmonary small vessel is a commonly used treatment protocol for patients with obstruction were reduced in the mice treated with salmeterol COPD (11,12). In addition, Frampton (13) have reported and/or formoterol, suggesting that salmeterol and formoterol that the combined use of inhaled formoterol and the corti- were beneficial for ongoing airway and blood vessel remodeling costeroid mometasone significantly improved the lung in mice with COPD. The most common treatment‑associated function in patients with asthma. Furthermore, Yip et al (14) adverse events were hypertension and proteinuria. In conclu- evaluated the effect of changing from fluticasone/salmeterol sion, combined salmeterol and formoterol treatment was more to mometasone/formoterol treatment in patients with COPD effective compared with either single agent, suggesting that and identified that patients experienced COPD exacerbation salmeterol and formoterol combined treatment has therapeutic after this conversion. However, the underlying mechanism of value for the clinical treatment of patients with COPD. the effect of combined salmeterol and formoterol treatment in COPD is not well understood, and few reports have evaluated Introduction its efficacy in preclinical and clinical trials. In the current study, the therapeutic efficacy of salmeterol Chronic obstructive pulmonary disease (COPD), also known as and formoterol was evaluated in mice with COPD induced by obstructive emphysema, is caused by the narrowing of airways airway lipopolysaccharide (LPS) inhalation. The therapeutic and lung damage (1,2). In recent years, the incidence of COPD efficacy and side effects of this treatment were evaluated in has increased markedly due to air pollution, smoking and a 56-day-long observation. Although salmeterol/formoterol chronic bronchitis (3). The symptoms of COPD cause a large is not currently approved for COPD therapy by the US global burden of disease (1,4). COPD also has a notable impact Food and Drug Administration, evidences from clinical on the quality of life of patients, frequently leading to the trials of mometasone/formoterol and salmeterol/formoterol have indicated that salmeterol/formoterol treatment is well tolerated and could improve lung function in patients with COPD (15,16). Based on previous clinical data (9), a combined salmeterol/formoterol therapeutic approach was designed to Correspondence to: Professor Xiaoli Yang, Department of Lung Disease, Yucheng City People's Hospital, 127 Nanyang Road, treat mice with COPD. Dezhou, Shangdong 350076, P.R. China E‑mail: [email protected] Materials and methods Key words: chronic obstructive pulmonary disease, salmeterol, Ethics statement. The present study was approved by the formoterol Ethics Committee of Yucheng City People's Hospital (Dezhou, China; Approval number: YCCPH: 20130567LPX1) and performed in accordance with the recommendations of the WANG et al: EFFICACY OF SALMETEROL AND FORMOTEROL FOR COPD THERAPY 1539 Guide for the Care and Use of Laboratory Animals of Yucheng Experimental mice were administered with drugs once daily City People's Hospital. All surgery and euthanasia procedures for a total of 56 days. The therapeutic effects of salmeterol were performed under intraperitoneal injection of sodium and/or formoterol on mice with COPD were measured as pentobarbital anesthesia (50 mg/kg), and all efforts were made described previously (21). to minimize suffering. Pulmonary function test. The pulmonary function of the mice Cell culture. MRC‑5 normal lung fibroblast cells were obtained after treatment with salmeterol and/or formoterol was assessed from the American Type Culture Collection (Manassas, VA, by recording changes in airway resistance and functional USA). The cells were cultured in Dulbecco's modified Eagle's residual capacity using a Buxco Pulmonary Mechanics system medium supplemented with 10% heat‑inactivated fetal bovine (Buxco Electronics, Inc., Wilmington, NC, USA) according serum (Lonza Group, Inc., Walkersville, MD, USA), 3 mM to the manufacturer's protocol. The efficacy of salmeterol L-glutamine, 50 µg/ml gentamicin and 1% penicillin/strepto- and/or formoterol on mice with COPD was analyzed by COPD mycin. All cells were cultured at 37˚C and in 5% CO2. MRC-5 assessment test scores (22). The severity is determined based cell models of COPD were established through 48 h incubation on score: low, <4, medium, ≥4 and <9 and high, ≥9. of LPS (2.5 mg/kg, Sigma‑Aldrich; Merck KGaA, Darmstadt, Germany). The MRC‑5 cells (MOCK), and LPS‑induced Histopathology. Hypertrophy and hyperplasia of the goblet MRC‑5 cells were treated with PBS (Control), salmeterol cells on airway surfaces, inflammatory cell infiltration, (0.16 mg/ml) and/or formoterol (0.32 mg/ml) for 24 h at 37˚C alveolar structural changes, and airway smooth muscle and for further analysis. intima cells were examined in the lungs of experimental mice by histopathology. On day 28, lung tissue samples were Reverse transcription‑quantitative polymerase chain reaction removed from the central airway, as previously described (23), (RT‑qPCR) analysis. Total RNA was extracted from MRC‑5 then sectioned, fixed with 4% paraformaldehyde at 4˚C for lung cells after treatment with salmeterol and/or formoterol 12 h. Lung tissues were embedded in paraffin and cut into using an RNeasy Mini kit (Qiagen Sciences, Inc., Gaithersburg, 4 µm thick sections for hematoxylin and eosin staining at 37˚C MD, USA) according to the manufacturer's protocol. Total for 2 h. Lung tissue sections were also stained with masson RNA (1 µg) was reverse transcribed into cDNA using a staining for 2 h at 37˚C to analyze the efficacy of salmeterol QuantiTect Reverse Transcription kit (Cat no. 205310; Qiagen and/or formoterol, according to previous study (24). Sciences, Inc.) according to the manufacturer's protocol. The cDNA (10 ng) was subjected to qPCR using SYBR Green Statistical analysis. All data are presented as the mean ± stan- Master mix (Bio‑Rad Laboratories, Inc., Hercules, CA, USA). dard error of the mean. Differences between groups were The reaction conditions were performed as follows: 95˚C for compared using an unpaired Student's t‑test. Comparisons 10 min and 35 cycles of 95˚C for 20 sec and 58˚C for 1 min. between multiple groups were performed using analysis of the Relative mRNA expression changes were calculated using the one‑way ANOVA variance. Analyses were performed using 2-∆∆Cq method (17). The results are expressed as a fold of the SPSS 19.0 (IBM Corp., Armonk, NY, USA) and GraphPad control. All primers were synthesized by Invitrogen; Thermo Prism 5 software (version 5.0; GraphPad Software, Inc., La Fisher Scientific, Inc. and are presented in Table I. Jolla, CA, USA). *P<0.05 and **P<0.01 was considered to indicate a statistically significant difference. Evaluation of toxicity. Toxicity was graded using the National Cancer Institute Common Toxicity Criteria (CTC; Results version 3.0) (18). Mice received 0.08, 0.16, 0.32 or 0.40 mg salmeterol or formoterol once a day for a total of 10 days (n=5 Duration of treatment and MTD of salmeterol and for in each group). Hypertension, diarrhea, proteinuria, vomiting, moterol. All mice salmeterol and/or formoterol (n=16/group). lethargy, rash, fatigue, constipation, weight, appetite, epistaxis, The median overall duration of treatment for the mice was hypertriglyceridemia and peripheral edema were evaluated 10 days for this analysis. Mice received 0.08, 0.16, 0.32 or and recorded every 2 days during therapy. A dose-limiting 0.40 mg of salmeterol or
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