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Updated: Jan 3, 2026

The Pilocarpine Model of Temporal Lobe Epilepsy and EEG Monitoring Using Radiotelemetry System in Mice
Published on: February 27, 2018
Rosiglitazone polarizes microglia and protects against pilocarpine-induced status epilepticus
Jing Peng1, Kan Wang1, Weiwei Xiang1
1Department of Neurology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
Aims:
Activated microglia have been found in the forebrains and hippocampi of temporal lobe epilepsy (TLE) patients and status epileptic (SE) animal models. The peroxisome proliferator-activated receptor γ (PPAR γ) agonist rosiglitazone has been shown to prevent microglial activation. However, its role in pilocarpine-induced status epilepticus remains unknown. We aimed to examine the effect of the PPAR γ agonist rosiglitazone in protecting against pilocarpine-induced status epileptic resulting from over-activation and to explore phenotypic changes in microglia as the underlying mechanism.
Methods:
Male C57BL/6 mice were assigned to three groups: the control group, pilocarpine-induced (SE) group, and rosiglitazone-treated (SE+Rosi) group. Status epileptic mice were administered 300 mg/kg pilocarpine via intraperitoneal injection. SE+Rosi mice were administered rosiglitazone (0.1 mg/kg, i.p.) after SE. Flow cytometry, immunofluorescence staining, and quantitative real-time PCR were used to examine the activation of and phenotypic changes in microglia in the brain and to evaluate neuroinflammation.
Results:
We found that the expression of proinflammatory CD86 and iNOS was increased and that the expression of antiinflammatory CD206 and Arg-1 was decreased in the brains of pilocarpine-induced SE mice compared to control mice. The mRNA levels of proinflammatory and antiinflammatory cytokines were not significantly changed in the brain. Rosiglitazone treatment significantly inhibited the proinflammatory polarization of microglia and rescued neuron loss in the temporal lobe and hippocampi of the brain after SE.
Conclusion:
Rosiglitazone reverses microglial polarization in the brains of SE mice and also affords neuroprotection against pilocarpine-induced status epilepticus without inducing significant changes in brain inflammation.
Insights
Rosiglitazone, a PPAR γ agonist, reversed harmful microglial polarization in mice with status epilepticus (SE). This treatment protected neurons in the temporal lobe and hippocampi, offering neuroprotection against SE.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Activated microglia are implicated in temporal lobe epilepsy (TLE) and status epilepticus (SE).
- Peroxisome proliferator-activated receptor γ (PPAR γ) agonists, like rosiglitazone, can inhibit microglial activation.
- The effect of rosiglitazone on pilocarpine-induced SE is not well understood.
Purpose of the Study:
- To investigate the neuroprotective effects of rosiglitazone in a pilocarpine-induced SE model.
- To explore the underlying mechanism involving microglial phenotypic changes.
Main Methods:
- Mice were divided into control, SE, and SE+rosiglitazone groups.
- SE was induced using pilocarpine (300 mg/kg, i.p.).
- Rosiglitazone (0.1 mg/kg, i.p.) was administered to the SE+Rosi group.
- Microglial activation, phenotype, and neuroinflammation were assessed using flow cytometry, immunofluorescence, and qPCR.
Main Results:
- SE mice showed increased proinflammatory markers (CD86, iNOS) and decreased anti-inflammatory markers (CD206, Arg-1) in the brain.
- Rosiglitazone treatment inhibited proinflammatory microglial polarization.
- Rosiglitazone treatment rescued neuron loss in the temporal lobe and hippocampi.
Conclusions:
- Rosiglitazone effectively reverses microglial polarization in SE mouse brains.
- This agent provides neuroprotection against pilocarpine-induced SE.
- Neuroprotection occurs without significant alteration of overall brain inflammation.
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