Introduction to Animal Models of Sepsis-Induced Brain Injury

The Aniphe BioLab animal model of sepsis‑induced brain injury is constructed based on core pathogenic mechanisms, including systemic inflammatory dysregulation, disruption of the blood–brain barrier, and amplification of neuroinflammatory cascades. Sepsis is primarily induced by infection or endotoxin administration, mimicking the dissemination of systemic inflammation into the central nervous system and leading to pathological changes such as cerebral microvascular damage, glial cell activation, and neuronal dysfunction. This model accurately reflects the onset and progression of sepsis‑associated encephalopathy (SAE).

Service Advantages of the Aniphe BioLablogical Sepsis-Induced Lung Injury Animal Model Platform

Leveraging a well-established platform of inflammatory and infectious disease models and a standardized experimental system, Aniphe BioLab offers a high‑quality, one‑stop in vivo model platform that is both standardized and reproducible, supporting research into the mechanisms of sepsis‑associated brain injury and the evaluation of neuroprotective therapeutics.

	The model has been built to be mature and stable. A classic sepsis-induction protocol was employed, resulting in a high model success rate and a stable neuroinflammatory phenotype.
	The brain injury phenotype is well-defined and controllable. It can reliably induce hallmark alterations, including blood–brain barrier disruption, neuroinflammation activation, and cognitive dysfunction.
	Refinement of the multidimensional evaluation system A comprehensive analysis integrating brain tissue pathology, inflammatory cytokine assays, and behavioral/cognitive function assessments.
	Adaptable to multi-phase research needs Supports research on the distinct stages of acute neuroinflammatory injury and subsequent cognitive dysfunction.
	Complete data delivery specifications Providing raw experimental data, brain tissue pathology images, and systematic analysis reports to ensure data traceability and compliance with publication‑grade standards.

Modeling cycle	1–2 weeks
Laboratory animals	Mice and rats of SPF grade
Positive drug	Commonly used agents such as dexamethasone, edaravone, minocycline, and dexmedetomidine are employed for evaluating anti-inflammatory, antioxidant, and neuroprotective effects.
Application areas	It is widely used in studies of the pathogenesis of sepsis‑associated encephalopathy, in elucidating neuroinflammatory pathways, in investigating the mechanisms of blood–brain barrier disruption, and in evaluating the pharmacodynamics of neuroprotective agents.

Establishment of an Animal Model of Sepsis-Induced Brain Injury

It is primarily established via cecal ligation and puncture (CLP) or intraperitoneal injection of lipopolysaccharide (LPS): In the CLP model, the distal segment of the cecum is ligated, and a perforation is created distal to the ligation site, allowing continuous leakage of intestinal contents into the peritoneal cavity, thereby triggering progressive polymicrobial infection and systemic inflammatory responses, which in turn induce sepsis and secondary brain inflammation–related injury. The LPS‑intraperitoneal injection model, by contrast, employs a single or multiple doses of lipopolysaccharide to rapidly activate TLR4‑mediated innate immune responses, precipitating a systemic cytokine storm and increased blood–brain barrier permeability, ultimately leading to neuroinflammation and neuronal dysfunction. These two approaches respectively mimic the pathophysiological processes underlying chronic infection‑type and acute endotoxin‑induced septic brain injury.