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.

中文翻译：

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罗格列酮可使小胶质细胞极化，并防止毛果芸香碱引起的癫痫持续状态。

AIMS激活的小胶质细胞已发现在颞叶癫痫（TLE）患者的前脑和海马和状态癫痫（SE）动物模型中。过氧化物酶体增殖物激活受体γ（PPARγ）激动剂罗格列酮已被证明可预防小胶质细胞的激活。然而，其在毛果芸香碱引起的癫痫持续状态中的作用仍是未知的。我们旨在研究PPARγ激动剂罗格列酮在预防由过度活化导致毛果芸香碱引起的状态癫痫中的作用，并探讨小胶质细胞的表型变化是其潜在机制。方法将雄性C57BL / 6小鼠分为三组：对照组，毛果芸香碱诱导（SE）组和罗格列酮治疗（SE + Rosi）组。地位性癫痫小鼠通过腹膜内注射给予300 mg / kg毛果芸香碱。SE + Rosi小鼠在SE后服用罗格列酮（0.1 mg / kg，ip）。流式细胞仪，免疫荧光染色和定量实时PCR用于检查大脑小胶质细胞的激活和表型变化，并评估神经炎症。结果我们发现毛果芸香碱诱导的SE小鼠大脑中促炎性CD86和iNOS的表达增加，而抗炎性CD206和Arg-1的表达与对照小鼠相比降低。大脑中促炎和抗炎细胞因子的mRNA水平没有显着变化。罗格列酮治疗显着抑制小胶质细胞的促炎性极化，并挽救了SE后脑颞叶和海马神经元的丢失。