Chronic Obstructive Pulmonary Disease (COPD) Animal Model
Chronic Obstructive Pulmonary Disease (COPD) Animal Model
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Chronic Obstructive Pulmonary Disease
Introduction to COPD Animal Models
Chronic obstructive pulmonary disease (COPD) is a common, highly prevalent chronic respiratory disorder characterized by persistent airflow limitation and chronic inflammation, primarily affecting the airways and alveoli and leading to progressive dyspnea.
Its onset is associated with an abnormal inflammatory response of the lungs to harmful gases or particles. Smoking and air pollution are the most common causes of chronic obstructive pulmonary disease, and the resulting damage to lung architecture is typically irreversible, requiring long-term management.
Advantages of Aniphe BioLab’s COPD Animal Model Platform Services
Aniphe BioLab’s animal model platform for chronic obstructive pulmonary disease (COPD), supported by a standardized modeling system, comprehensive assay capabilities, and an SPF‑grade experimental facility, offers end‑to‑end services—from model establishment to efficacy evaluation—thereby advancing research into the pathogenesis of respiratory diseases and facilitating drug discovery.
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The modeling protocol is well-established. By employing the classic smoke‑exposure combined with airway irritation modeling method, models of varying severity can be established, with stable and highly reproducible outcomes. |
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The testing system has been improved. It encompasses a range of assays, including pulmonary function tests, pathological staining, and inflammatory cytokine measurements, to provide a comprehensive evaluation of the model and drug efficacy. |
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Experimental quality control is stringent. Leveraging SPF-grade facilities, we support large-scale model generation and ensure the accuracy and reliability of experimental data. |
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Comprehensive and flexible services We offer end-to-end experimental services, with customizable solutions tailored to meet the needs of diverse research settings. |
| Modeling cycle |
4 weeks |
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Male Balb/c mice or SD rats |
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Fluticasone, a glucocorticoid, combined with salmeterol, a long-acting β₂‑adrenergic agonist, was used as the positive control. |
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It is primarily used to investigate the pathogenic mechanisms of chronic obstructive pulmonary disease, as well as the patterns of airway remodeling and inflammatory progression. Additionally, it is widely employed in the screening, efficacy evaluation, and safety assessment of candidate drugs targeting anti‑inflammation, bronchodilation, and improvement of pulmonary function. It can also facilitate the development and preclinical validation of novel drug delivery systems and therapeutic strategies. |
Experimental results
Construction of an Animal Model of COPD
Modeling principle: By intranasal instillation of bacterial lipopolysaccharide (LPS) and long-term passive inhalation of cigarette smoke, pathological changes such as airway epithelial injury, inflammatory cell infiltration, and alveolar destruction are induced in mice, thereby mimicking the pathogenesis of COPD.
Operational guidelines: The LPS dose should be moderate, and the infusion must be administered slowly to prevent coughing, which could lead to uneven drug distribution.
Smoking chamber: Must be airtight with controllable ventilation, ensuring uniform distribution of smoke concentration to prevent excessive levels that could lead to acute carbon monoxide or nicotine poisoning, and allowing easy observation of the mice’s condition.
General observation
Sham group: In normal mice, there were no deaths; the fur was glossy, breathing was regular, and activity was normal.
COPD group: Mice exhibited dull, lusterless fur, lethargy, and restlessness; they tended to huddle together when exposed to smoke, with rapid breathing, and in severe cases, obvious open-mouth breathing.
Pulmonary function testing
01 Pulmonary function indices: The decline in the ratio of forced expiratory volume in one second to forced vital capacity (FEV0.1/FVC) serves as the core indicator, reflecting the degree of airway obstruction and constituting a key functional measure for assessing COPD.
Airway resistance in mice was measured, and the FEV0.1/FVC ratio (forced expiratory volume in 0.1 seconds to forced vital capacity) was calculated to assess airway obstruction. As shown in the figure, the FEV0.1/FVC ratio was markedly reduced in the COPD group, indicating the presence of irreversible airway obstruction.

Image source: Aniphe BioLab
02 Pulmonary histopathology: Using disorganized alveolar architecture, alveolar enlargement, rupture and fusion of alveolar walls, and a reduced alveolar count as the gold standard, supplemented by inflammatory marker assessment, to ensure that the model exhibits COPD‑specific features at both the functional and structural levels.
HE staining revealed that, in the COPD group, the alveolar architecture was disorganized, with extensive inflammatory cell infiltration, tracheal wall thickening, alveolar cavity enlargement, and disruption and fusion of alveolar walls—pathological changes characteristic of the condition.

Image source: Aniphe BioLab
03 Flow cytometric analysis of bronchoalveolar lavage fluid: Bronchoalveolar lavage fluid is obtained as follows: After euthanizing the mice, perform bronchoalveolar lavage on the lung tissue by instilling 1 mL of pre‑cooled PBS into the lungs and rinsing three times. Collect the lavage fluid in a centrifuge tube and centrifuge at 4 °C, 1,000 r/min, for 10 minutes. Note: The lavage flushes only the luminal contents; proceed gently.
Flow cytometry analysis of bronchoalveolar lavage fluid revealed that, compared with the sham control group, the COPD model group exhibited significantly elevated proportions of leukocytes, alveolar macrophages, and neutrophils, indicating substantial recruitment of inflammatory cells into the airways of the model animals—consistent with the hallmark airway inflammation observed in COPD.

Image source: Aniphe BioLab
Detection of inflammatory markers and oxidative stress biomarkers
01 Inflammatory marker assessment: Serum levels of the pro-inflammatory cytokines TNF-α, IL-6, and IL-1β are measured; these markers reflect the extent of inflammation.
02 Oxidative stress biomarkers: Assessment of oxidative stress indicators such as malondialdehyde (MDA) and superoxide dismutase (SOD) in lung tissue.
Inflammation Level Analysis—ELISA: In the COPD group, the levels of the inflammatory mediators TNF-α, IL-6, and IL-1β were elevated.

Image source: Aniphe BioLab
Selection of Positive Control Drugs
01 Drug Selection
Fluticasone, a glucocorticoid, combined with salmeterol, a long-acting β₂‑adrenergic agonist, was used as the positive control and was administered for 2–3 weeks.
It is supported by robust clinical evidence and is a first-line therapy for COPD.
02 Mechanism of Action of Drugs
This combination therapy can significantly improve pulmonary function and reduce acute exacerbations, providing a quantitative benchmark for novel interventions.
HE staining results showed that, compared with the COPD group, the positive control group exhibited less disorganization of alveolar architecture, reduced inflammatory cell infiltration, thinner tracheal walls, enlarged alveolar spaces, and fewer instances of alveolar wall rupture and fusion.

Image source: Aniphe BioLab
















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