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Cerebral ischemia MCAO animal model

Cerebral ischemia MCAO animal model

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Hemorrhagic stroke
Psychiatric & neurological disease models

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Model Introduction

Model Introduction

Platform Service Advantages

Platform Service Advantages

Experimental results

Experimental results

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Hemorrhagic stroke

Introduction to Animal Models of Cerebral Ischemia

The middle cerebral artery (MCA) is a common site of stroke; accordingly, the MCA occlusion (MCAO) animal model is an internationally recognized standard for focal cerebral ischemia, with pathogenic mechanisms that closely resemble those of human ischemic stroke. The primary methods for establishing this model include craniotomy‑based mechanical occlusion, photochemical induction, filament‑thread embolization, and thromboembolic occlusion. Among these, filament‑thread embolization has become the most widely used approach in recent years. This technique avoids craniotomy and does not require ventilatory support or other specialized equipment, yields a relatively consistent ischemic region, allows precise control over the duration of ischemia and reperfusion, facilitates fine-tuning of local conditions, and minimizes systemic effects, making it the preferred method for generating models of focal cerebral ischemia–reperfusion injury.

Service Advantages of the Aniphe BioLab Cerebral Ischemia Animal Model Platform

Leveraging a well-established MCAO modeling system and extensive experience in stroke research, we provide a rapid, robust, and highly reproducible in vivo platform for investigating the mechanisms of cerebral ischemia and evaluating neuroprotective agents.

Comprehensive model coverage

Classic model

The filament occlusion method (MCAO) is used to establish the model, which avoids craniotomy, minimizes animal trauma, and yields highly reproducible results.
Standardization of the modeling process

Stable and reliable

Standardized surgical protocols, combined with an experienced technical team, ensure the stability and consistency of model creation.
Multidimensional Evaluation System

Multidimensional verification

The Longa score and the Bederson score, combined with TTC staining, were used to comprehensively validate the model’s phenotype.
Adapted for multi-cycle studies

Full-process traceability

Retain photographs of key procedural milestones and original records to ensure traceability of the experimental process.
Standardization of Data Delivery

Fast delivery

A standardized in vivo solution that meets the needs of cerebral ischemia mechanism research and drug efficacy evaluation.
Modeling cycle 24 hours, 3 days or 7 days

1  Laboratory animals

Mice and rats of SPF grade

1  Positive drug

Edaravone, butylphthalide, nimodipine

1  Application areas

Evaluation of the therapeutic efficacy of traditional Chinese medicines for stroke, neuroprotective research, mechanisms of cerebral ischemia-reperfusion injury, and assessment of stem cell/exosome-based therapies.

Experimental results

Construction of an MCAO animal model

Thread‑tack method: Perform ligation below the common carotid artery and at the external carotid artery, and place a preliminary thread at the proximal end of the common carotid artery.

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Photos of key steps in model creation

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Behavioral testing

Scoring should be performed 24 hours after the onset of ischemia in animals; two primary methods are used: the Longa scale and the Bederson scale. Phenotypic analysis: contralateral circling.

0 points: No symptoms of nerve injury
1 point: Unable to fully extend the contralateral forelimb.
2 points: Turn in a circle to the opposite side.
3 points: Tilt to the opposite side
4 points: Unable to walk independently; loss of consciousness; TTC staining of brain tissue.

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TTC staining of brain tissue

TTC staining revealed prominent white infarct foci in the brain tissue sections of the model group, indicating successful establishment of the cerebral ischemia model. In the treatment group, the infarct area was significantly reduced compared with the model group, suggesting that the drug effectively attenuates brain tissue damage induced by cerebral ischemia.

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Precautions

01 After surgery, it is important to stay warm. Mice during and after the ischemic period should be heated on a heating stage set to 38°C.
02 During the procedure, within the ischemic time frame, Physiological saline should be applied to the wound to keep it moist and prevent it from drying out.
03 Postoperative Care: On the day of model induction, antibiotics must be administered: Bayli 0.1 ml of stock solution diluted 50-fold, at a dose of 10 µl/g.
04 Postoperatively, goat milk powder must be administered via gavage daily. 3–4 times, with 0.5 mL administered by gavage each time.

Data on the treatment with butylphthalide (NBP)

01 Cerebral Edema and Blood–Brain Barrier Permeability Assay in Brain Tissue

Compared with the Sham group, the I/R group exhibited a significant increase in brain water content (P < 0.01); compared with the I/R group, the NBP‑preconditioned group showed a significant reduction in brain water content (P < 0.01). Compared with the Sham group, the I/R group demonstrated a significant elevation in brain EB content (P < 0.01); compared with the I/R group, the NBP‑preconditioned group exhibited a significant decrease in brain EB content (P < 0.01). 1

02 Immunohistochemical Test Results

Compared with the sham‑operation group (0.27 ± 0.03), the model group exhibited a significantly increased mean optical density of MMP‑9–positive expression in brain tissue (0.48 ± 0.07). In contrast, compared with the model group, the NBP‑preconditioned group showed a markedly reduced mean optical density of MMP‑9–positive expression in brain tissue (0.35 ± 0.05) (P < 0.01).

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03 Western Blot Results

Compared with the sham‑operation group (0.41 ± 0.04), the model group exhibited a significantly increased mean optical density of MMP‑9–positive expression in brain tissue (1.12 ± 0.17). In contrast, compared with the model group, the NBP pretreatment group showed a markedly reduced mean optical density of MMP‑9–positive expression in brain tissue (0.48 ± 0.05) (P < 0.01).

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References: The protective effects of butylphthalide pretreatment on cerebral ischemia-reperfusion injury in rats and its possible mechanisms.