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Respiratory Distress Syndrome (RDS) animal model
Respiratory Distress Syndrome (RDS) animal model
Publish an article
Respiratory Distress Syndrome
Introduction to RDS Animal Models
Respiratory Distress Syndrome (RDS) is an acute respiratory disorder characterized primarily by deficiency or dysfunction of pulmonary surfactant, decreased lung compliance, and severe hypoxemia, which can lead to diffuse alveolar injury, impaired gas exchange, and respiratory failure. Animal models of RDS can be established through methods such as depletion of pulmonary surfactant, lipopolysaccharide (LPS) administration, hydrochloric acid (HCl) instillation, or mechanical ventilation–induced lung injury. These models effectively mimic key pathological processes, including lung injury, inflammatory responses, and respiratory dysfunction, and are widely used in studies of the pathogenesis of RDS.
Advantages of Aniphe BioLab’s RDS Animal Model Platform Services
Leveraging a well-established RDS animal model platform, Aniphe BioLab provides clients with stable, reliable, one-stop pharmacological efficacy evaluation services.
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The model is mature and stable. It encompasses classic RDS models such as LPS, hydrochloric acid infusion, and mechanical injury, with high reproducibility. |
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The evaluation system has been improved. Supports multi-dimensional assessments, including pulmonary function testing, blood gas analysis, histopathology, and inflammatory cytokine assays. |
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Flexible, customized solutions It meets diverse needs, including pharmacological efficacy evaluation, mechanistic studies, and target validation. |
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Standardized Quality Control Standardized end-to-end operations ensure model stability and data integrity. |
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The filament occlusion method (MCAO) is used to establish the model, which avoids craniotomy, minimizes animal trauma, and yields highly reproducible results. |
Standardized surgical protocols, combined with an experienced technical team, ensure the stability and consistency of model creation. |
The Longa score and the Bederson score, combined with TTC staining, were used to comprehensively validate the model’s phenotype. |
Retain photographs of key procedural milestones and original records to ensure traceability of the experimental process. |
A standardized in vivo solution that meets the needs of cerebral ischemia mechanism research and drug efficacy evaluation. |
| Modeling cycle | 1–2 weeks |
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Mice and rats of SPF grade |
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Dexamethasone, budesonide, and pulmonary surfactant preparations are commonly used as positive controls for evaluating the anti-inflammatory and lung-protective effects of drugs. |
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It is primarily used for research on the pathogenesis of RDS, screening of anti-inflammatory and lung-protective drugs, evaluation of pulmonary surfactants, optimization of respiratory support strategies, and preclinical studies of innovative therapies. |
Construction of ROS Animal Models
An acute lung injury model can be established by intratracheal instillation of LPS, which induces pulmonary inflammation, alveolar structural damage, and pulmonary edema, thereby reliably mimicking the pathophysiological processes of RDS. This model is characterized by rapid establishment and excellent reproducibility, making it widely used in studies of disease mechanisms as well as in the evaluation of the efficacy of anti-inflammatory and lung-protective drugs.
Pyridostigmine Treatment Data
01 Quantitative analysis of BAL cells in 72-hour persistent LPS‑induced lung injury revealed that pyridostigmine alone did not elicit pulmonary inflammation. In the LPS model group, alveolar inflammatory cell populations were markedly increased; pyridostigmine treatment significantly reduced the total cell count as well as the numbers of neutrophils, macrophages, and lymphocytes, thereby comprehensively suppressing inflammatory cell infiltration into the lungs.
02 The results of the 72-hour persistent LPS-induced lung injury model showed that LPS can induce extensive neutrophil infiltration in lung tissue; pyridostigmine treatment significantly reduced pulmonary neutrophil density and ameliorated alveolar architecture as well as inflammatory pathological changes in the lungs.
03 Cell staining of bronchoalveolar lavage fluid revealed that LPS stimulation markedly recruits neutrophils, macrophages, and lymphocytes; pyridostigmine treatment significantly reduces the numbers of these three types of inflammatory cells and effectively suppresses pulmonary inflammatory cell infiltration during both the acute phase at 24 hours and the protracted phase at 72 hours.
References: The Cholinergic Drug Pyridostigmine Alleviates Inflammation During LPS-Induced Acute Respiratory Distress Syndrome.
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Phone:025-8520 8061
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