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Animal model of traumatic brain injury

Animal model of traumatic brain injury

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Traumatic brain injury
Psychiatric & neurological disease models

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Model Introduction

Model Introduction

Platform Service Advantages

Platform Service Advantages

Model Construction

Model Construction

Treatment data

Treatment data

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Traumatic brain injury

Introduction to Animal Models of Traumatic Brain Injury

Animal models of traumatic brain injury (TBI) constitute a classic experimental framework that mimics the pathophysiological processes of human cranial–brain trauma through mechanical external forces. Common modeling techniques include controlled cortical impact (CCI), fluid‑impulse injury (FPI), and weight‑drop injury. At their core, these methods involve applying a precisely controllable physical insult to a specific brain region under anesthetized conditions, thereby inducing either focal or diffuse brain tissue damage. Following model establishment, hallmark pathological changes—such as blood–brain barrier disruption, neuronal death, neuroinflammatory responses, and glial cell activation—can be observed, making these models widely employed in studies of neuroprotective mechanisms and in the in vivo evaluation of the efficacy of anti‑inflammatory and anti‑apoptotic therapeutics.

Advantages of Aniphe Aniphe Biolaboratory's TBI Animal Model Platform Services

Aniphe Biolaboratory animal model platform for traumatic brain injury (TBI) is centered on controllable injury severity and highly reproducible neuropathological reconstruction, providing a stable and reliable in vivo evaluation system for the development of neuroprotective and reparative therapeutics.

Comprehensive model coverage

Mature multi-type modeling approaches

It supports mainstream TBI models, including controlled cortical impact (CCI), fluid percussion injury (FPI), and weight-drop injury, covering both focal and diffuse injury types.
Standardization of the modeling process

Damage parameters can be precisely controlled.

Key parameters such as impact depth, velocity, and pressure are standardized to enable hierarchical modeling of varying damage severities.
Multidimensional Evaluation System

The model exhibits high reproducibility.

The extent and severity of nerve injury remain stable, thereby reducing data variability attributable to individual differences.
Adaptable to multi-cycle studies

Pathological features closely resemble clinical findings.

It can reliably reproduce the typical pathological processes, including blood–brain barrier disruption, neuronal loss, axonal damage, and neuroinflammatory responses.
Standardization of Data Delivery

The multi-dimensional evaluation system has been refined.

Systematic pharmacological efficacy validation is achieved through a combination of behavioral assessments, imaging analyses, and histopathological examinations.
Modeling cycle

24–32 weeks

1  Laboratory animals

C57BL/6J mice

1  Positive drug

There is currently no unified gold standard; the commonly used positive drug is edaravone.

1  Application areas

Mechanisms of secondary brain injury (neuroinflammation, oxidative stress, glutamatergic excitotoxicity), screening of neuroprotective agents, identification of biomarkers, research on neurological rehabilitation and regeneration, and studies on traumatic brain injury complicated by multiple organ dysfunction.

Construction of an Animal Model of Traumatic Brain Injury

01 Controlled Cortical Impact (CCI)

A precise, reproducible focal brain injury is induced by delivering controlled impacts to the exposed cortical surface using electromagnetic or pneumatic devices, with adjustable velocity, depth, and dwell time. This model features highly standardized parameters—such as velocity, depth, and dwell time—that can be finely tuned—resulting in a stable, well‑defined lesion area and robust experimental reproducibility. It is one of the most reproducible and standardized models for traumatic brain injury (TBI) research, making it well suited for mechanistic studies and pharmacological efficacy assessments.

02 Weight Drop Model

Different masses are dropped from a fixed height to impact the skull or dura mater, thereby inducing closed‑head traumatic brain injury. This method is advantageous because it is simple to perform, low in cost, and well suited for large‑scale experiments; however, due to rebound and secondary impacts, the consistency of the injury is relatively poor, making it commonly used for preliminary screening studies and basic pharmacological efficacy assessments.

03 Fluid Pressure Impact Method (FPI)

An instantaneous pressure wave is transmitted through a cranial window into the brain tissue via a hydraulic system, resulting in diffuse axonal injury and features of mixed traumatic brain injury. This model effectively mimics intracranial pressure fluctuations and the ensuing secondary brain injury process; however, it demands high operational precision and is well suited for studies on neuroprotection and the mechanisms of secondary injury.

 

Edaravone (EDA) treatment data

01 EDA treatment can ameliorate neurological deficits following traumatic brain injury in mice.

Twenty-four hours after the completion of model establishment in mice, a double-blind protocol was employed to assess neurological function. NSS scores revealed a significant reduction in the treatment group compared with the TBI group. To further confirm the neuroprotective effects of EDA following traumatic brain injury, brain tissues from mice receiving continuous drug administration for 7 days post-injury were subjected to hematoxylin–eosin staining. Under identical experimental conditions, the lesion area in the EDA-treated group was found to be smaller than that in the TBI group.

 

 

02 EDA treatment can attenuate the oxidative stress response in brain tissue induced by traumatic brain injury in mice.

To assess the reactive nitrogen species generated during the oxidative stress response induced by traumatic brain injury in mice, 3-nitrotyrosine (3-NT) was measured by Western blotting 24 hours after injury. Compared with the sham group, the TBI group exhibited a significant increase in 3-NT protein levels (P < 0.05), whereas the treatment group showed a significant reduction in 3-NT levels relative to the TBI group (P < 0.05).

 

 

To further validate the therapeutic effects of EDA, this study employed immunofluorescence staining to assess 3-NT expression; the results were consistent with those obtained by Western blotting, demonstrating that EDA treatment reduces 3-NT expression.

 

 

This study also measured tissue malondialdehyde (MDA) levels, and the results were consistent with expectations: MDA expression was significantly higher in the TBI group compared with the Sham group (P < 0.01), whereas MDA levels were reduced in the treatment group relative to the TBI group (P < 0.05).

 

 

03 EDA treatment in mice with traumatic brain injury can increase nuclear translocation of Nrf2 protein in brain tissue, thereby alleviating brain damage.

At 24 hours after traumatic brain injury in mice, Western blotting was used to assess the expression level of Nrf2 protein in cortical brain tissue nuclei. The TBI group exhibited higher Nrf2 protein expression than the Sham group, while the EDA‑treated group showed even greater Nrf2 expression compared with the TBI group; all differences were statistically significant.

 

 

To further validate this finding, this study employed RT‑qPCR to assess Nrf2 mRNA transcription. The results similarly demonstrated that the Nrf2 gene expression level was significantly higher in the TBI group compared with the Sham group (P < 0.05), and that the drug‑treated group exhibited even higher expression levels than the TBI group (P < 0.05).

 

 

To more directly assess the effects of EDA, immunofluorescence was used to examine Nrf2 protein expression. As shown in Figure 8, compared with the Sham group, the TBI group exhibited increased nuclear translocation of Nrf2; moreover, compared with the TBI group, the EDA group demonstrated even more pronounced nuclear accumulation of Nrf2.

 

References: The effect of edaravone on oxidative stress responses following traumatic brain injury in mice.