作者: Sheng-Wei Lai , Jia-Hong Chen , Hsiao-Yun Lin , Yu-Shu Liu , Cheng-Fang Tsai
DOI: 10.1007/S12035-018-0933-Z
关键词:
摘要: Inhibition of microglial over-activation is an important strategy to counter balance neurodegenerative progression. We previously demonstrated that the adenosine monophosphate-activated protein kinase (AMPK) may be a therapeutic target in mediating anti-neuroinflammatory responses microglia. Brain-derived neurotrophic factor (BDNF) one major factors produced by astrocytes maintain development and survival neurons brain, have recently been shown modulate homeostasis neuroinflammation. Therefore, present study focused on BDNF-mediated neuroinflammatory provide endogenous regulation Among tested neuroinflammation, epigallocatechin gallate (EGCG) minocycline exerted BDNF upregulation inhibit COX-2 proinflammatory mediator expressions. Furthermore, both EGCG upregulated expression microglia through AMPK signaling. In addition, also increased expressions erythropoietin (EPO) sonic hedgehog (Shh). modulation astrocyte-conditioned medium (AgCM) decreased The anti-inflammatory effects were mediated EPO/Shh Our results indicated BDNF-EPO-Shh novel-signaling pathway underlies inflammatory regarded as potential diseases. This reveals better understanding crosstalk between regulate actions, which could novel for treatment neuroinflammation