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首页> 外文期刊>Neuroscience: An International Journal under the Editorial Direction of IBRO >PI3Kgamma INHIBITION ALLEVIATES SYMPTOMS AND INCREASES AXON NUMBER IN EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS MICE
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PI3Kgamma INHIBITION ALLEVIATES SYMPTOMS AND INCREASES AXON NUMBER IN EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS MICE

机译：PI3Kamma抑制剂缓解了实验性自动免疫性脑脊髓炎小鼠的症状并增加了轴突数目

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摘要

Phosphoinositide 3-kinase y (PI3Ky) is a shared downstream component of chemokine-mediated signaling pathways and regulates migration, proliferation and activation of inflammatory cells. PI3Ky has been shown to play a crucial role in regulating inflammatory responses during the progression of several diseases. We investigated the potential function of PI3Ky in mediating inflammatory reactions and the development of experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS). We found that systemic treatment with selective PI3Ky inhibitor AS-604850 significantly reduced the number of infiltrated leukocytes in the CNS and ameliorated the clinical symptoms of EAE mice. Treatment with this PI3Ky inhibitor enhanced myelination and axon number in the spinal cord of EAE mice. Consistently, we demonstrated that PI3Ky deletion in knockout mice mitigates the clinical sign of EAE compared to PI3Ky+/+ controls.
机译：磷酸肌醇3-激酶γ（PI3Ky）是趋化因子介导的信号通路的下游共享成分，并调节炎症细胞的迁移，增殖和活化。已经证明PI3Ky在几种疾病的进展过程中在调节炎症反应中起关键作用。我们调查了PI3Ky在介导炎症反应和实验性自身免疫性脑脊髓炎（EAE），多发性硬化症（MS）模型的发展中的潜在功能。我们发现，使用选择性PI3Ky抑制剂AS-604850进行的全身治疗显着减少了CNS中浸润的白细胞数量，并改善了EAE小鼠的临床症状。用这种PI3Ky抑制剂治疗可增强EAE小鼠脊髓的髓鞘形成和轴突数量。一致地，我们证明了与PI3Ky + / +对照相比，基因敲除小鼠中的PI3Ky缺失减轻了EAE的临床症状。

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