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Parkinson’s disease PD animal model

Parkinson’s disease PD animal model

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Parkinson's disease
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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Parkinson's disease

Introduction to the PD Mouse Model

Parkinson’s disease (PD) is a neurodegenerative disorder that predominantly affects middle-aged and older adults, with its precise etiology still not fully elucidated. Clinically, PD patients typically present with bradykinesia, gait abnormalities, postural instability, and resting tremor. Pathologically, it is characterized by the degeneration of dopaminergic neurons and the formation of Lewy bodies. In animal models, MPTP is commonly used to induce PD in mice.

Advantages of Aniphe BioLab’s PD Mouse Model Platform Services

Leveraging years of experience in establishing Parkinson’s disease animal models, we deliver models with robust stability and high phenotypic consistency. By implementing standardized quality-control protocols to rigorously screen and select study animals, we provide efficient, reproducible in vivo research support for your preclinical efficacy assessments and new‑drug development.

Comprehensive model coverage

Clinically relevant

It replicates the typical pathological features and motor symptoms of PD, with a high degree of similarity.

Standardization of the modeling process

Stable and reliable

Standardized modeling with high success rates and excellent reproducibility.

Multidimensional Evaluation System

Comprehensive testing

Comprehensive multi-dimensional testing ensures data is standardized and usable.

Standardization of Data Delivery

High cost-performance ratio

Easy to raise, with a controllable life cycle and low overall costs.

Modeling cycle

7 days

1  Laboratory animals

C57 male mice

1  Positive drug

Berberine

1  Application areas

This model is primarily used to investigate disease pathogenesis, screen and evaluate neuroprotective drug candidates, and validate the efficacy of novel therapeutic approaches such as genetic, cellular, and physical interventions. It is also well suited for identifying pathological biomarkers and studying disease progression, thereby providing robust support for basic research and preclinical translation of new drugs.

Experimental results

Construction of a PD animal model

A mouse model of Parkinson’s disease was established by intraperitoneal injection of MPTP, administered four times daily at two-hour intervals for one day.

 

Histopathology

Nissl staining

Observation of neuronal morphology and quantitative changes in the substantia nigra revealed the following: in the control group, tissue sections exhibited uniformly intense staining, with numerous densely packed neurons and well-defined cellular outlines; in the model group, sections showed markedly lighter staining, a significant reduction in the number of substantia nigra neurons, loose cellular arrangement, and indistinct cellular contours, indicating damage to dopaminergic neurons in PD mice.

 

 

H&E staining

HE staining revealed that, in the control group, the neurons in the substantia nigra exhibited normal morphology, with a high cell density and orderly arrangement. In contrast, the model group showed a marked reduction in neuronal numbers, disorganized arrangement, and, in some cases, pyknosis of the neuronal soma and deeply stained cytoplasm, indicating the development of neuroinflammation in the PD mice.

 

 

Behavioral testing

Rotarod test

According to the rotarod analysis, the latency to fall was significantly shortened in the Parkinson’s disease model group, indicating impaired motor coordination.

 

 

Climbing pole experiment

According to the pole-climbing data, mice in the Parkinson’s disease model group exhibited significantly prolonged climbing times, indicating impaired motor coordination.

 

 

Precautions

1. Following MPTP injection, behavioral assessments should be conducted as soon as possible.

2. MPTP is highly toxic; personal protective measures should be observed during handling to avoid inhalation or skin contact.

3. The dose and administration frequency of MPTP should be determined based on the experimental objectives and the mice’s sensitivity; excessive dosing may result in mouse mortality.

4. Behavioral testing should be conducted in a quiet environment with soft lighting to minimize external distractions.

5. During histological analysis, it is essential to accurately label and localize brain structures to ensure data accuracy.

 

Berberine (BBR) treatment data

01 Locomotor Behavior and Body Weight Monitoring

BBR significantly ameliorates motor bradykinesia, muscle strength decline, reduced spontaneous locomotion, and weight loss in MPTP‑induced Parkinsonian mice, whereas the autophagy inhibitor 3‑MA completely abolishes BBR’s neuroprotective effects, demonstrating that BBR’s alleviation of PD‑related motor deficits depends on activation of the autophagy pathway.

 

 

02 Immunohistochemistry and Protein Quantification Assays

BBR can protect dopaminergic neurons in the nigrostriatal pathway, enhance dopamine transporter and receptor protein expression, and alleviate MPTP‑induced damage to the dopaminergic system. The autophagy inhibitor 3‑MA completely abolishes BBR’s neuroprotective effects, demonstrating that BBR’s protective action against Parkinsonian injury depends on the activation of the autophagy pathway.

 

 

03 Immunofluorescence and Protein Quantification Assays

BBR markedly suppresses MPTP‑induced excessive activation of astrocytes and microglia in the substantia nigra of Parkinson’s disease mice, thereby alleviating central nervous system inflammation. This protective effect is abolished upon inhibition of the autophagy pathway, demonstrating that BBR’s suppression of neuroinflammation depends on its modulation of autophagic function.

 

 

04 NLRP3 Inflammasome Pathway Assay

Overall results indicate that BBR can inhibit MPTP‑induced excessive activation of the microglial NLRP3 inflammasome, reduce the release of downstream pro‑inflammatory proteins and cytokines, and alleviate substantia nigra–related neuroinflammation. Furthermore, the autophagy inhibitor 3‑MA completely abolishes the anti‑inflammatory effects of BBR, demonstrating that BBR’s suppression of the NLRP3 inflammasome depends on its ability to repair autophagic dysfunction.

 

References: Berberine Protects Against NLRP3 Inflammasome via Ameliorating Autophagic Impairment in MPTP-Induced Parkinson's Disease Model