Introduction to the ALI Animal Model

The acute lung injury (ALI) animal model is a classic experimental system used to mimic acute pulmonary inflammation and impaired gas exchange. It is commonly established by intratracheal instillation of lipopolysaccharide (LPS), bleomycin administration, mechanical ventilation–induced lung injury, or aspiration of acidic fluids. Following model induction, this approach leads to damage of alveolar epithelial and capillary endothelial cells, triggering extensive inflammatory cell infiltration, pulmonary edema, and alveolar collapse. These changes result in decreased lung compliance and compromised oxygenation, accompanied by elevated levels of pro-inflammatory cytokines such as TNF‑α and IL‑6, as well as increased oxidative stress. Consequently, the ALI model is widely employed for investigating the pathogenesis of acute lung injury and acute respiratory distress syndrome (ARDS), as well as for evaluating therapeutic agents.

Advantages of the ALI Animal Model Platform from Aniphe BioLab

The Aniphe BioLab Acute Lung Injury (ALI) animal model platform is centered on its ability to stably induce inflammation and reliably reproduce pulmonary functional impairment, providing a robust in vivo model system for studying the mechanisms of acute respiratory diseases and for evaluating anti-inflammatory and lung-protective therapeutics.

	Multiple modeling approaches are well-established. It encompasses models such as intravenous injection of oleic acid combined with lipopolysaccharide and cecal ligation and puncture (CLP).
	The inflammatory response is stable and controllable. By standardizing dosage and administration protocols, inflammatory intensity can be modulated, thereby enhancing model consistency and success rates.
	Pulmonary injury phenotype is stable. It reliably induces pulmonary edema, destruction of alveolar architecture, and impaired oxygenation—typical pathological features.
	The pathological mechanisms are closely aligned with clinical practice. It can reliably reproduce key processes such as inflammatory cell infiltration, cytokine storm, and oxidative stress.
	The model exhibits high reproducibility. Standardize operational procedures and rearing conditions to minimize batch-to-batch variability and enhance data comparability.
	The multi-dimensional evaluation system has been refined. Systematic assessment is achieved through the integration of pulmonary function testing, histopathological analysis, and inflammatory cytokine profiling.

Modeling cycle	1–3 days
Laboratory animals	C57BL/6 mice and SD rats
Positive drug	Dexamethasone (anti-inflammatory), ulinastatin (protease inhibitor), N-acetylcysteine (antioxidant), and others are used to assess the model’s responsiveness to anti-inflammatory and antioxidant therapies.
Application areas	Pathogenesis of ALI/ARDS (inflammation, barrier disruption, oxidative stress); screening of anti-inflammatory and lung-protective agents; preclinical evaluation of stem cell therapies (e.g., mesenchymal stem cells) and biologics.

Construction of the ALI animal model

In the oleic acid–lipopolysaccharide (OA+LPS) intravenous injection model, oleic acid is administered via the tail vein to induce microvascular thrombosis, while lipopolysaccharide is concurrently administered to activate a systemic inflammatory response. This leads to cerebral microcirculatory dysfunction, blood–brain barrier disruption, and neuroinflammation, ultimately resulting in impaired cognitive function. In the cecal ligation and puncture (CLP) model, surgical intervention induces intra-abdominal infection and sepsis, triggering a systemic inflammatory cascade and inadequate tissue perfusion, which in turn precipitates cerebral ischemia–hypoxia–induced injury, manifesting as deficits in learning and memory and neurological dysfunction.

Both models can reliably simulate the pathogenesis of brain injury under the interplay of inflammation and ischemia, characterized by neuroinflammatory activation, exacerbated oxidative stress, and synaptic dysfunction. They serve as valuable complementary platforms for investigating the mechanisms underlying vascular cognitive impairment and for developing therapeutic interventions.