Curcumin Attenuates gp120-Induced Microglial Inflammation by Inhibiting Autophagy via the PI3K Pathway
作者： Guiling Chen , Sisi Liu , Rui Pan , Guangming Li , Haijie Tang
DOI: 10.1007/S10571-018-0616-3
关键词:
摘要: Microglial inflammation plays an essential role in the pathogenesis of HIV-associated neurocognitive disorders. A previous study indicated that curcumin relieved microglial inflammatory responses. However, mechanism this process remained unclear. Autophagy is a lysosome-mediated cell content-dependent degradation pathway, and uncontrolled autophagy leads to enhanced inflammation. The curcumin-attenuating BV2 caused by gp120 was investigated with or without pretreatment inhibitor 3-MA blockers NF-κB, IKK, AKT, PI3K, we then detected production mediators monocyte chemoattractant protein-1 (MCP-1) IL17 using ELISA, markers ATG5 LC3 II Western Blot. autophagic flux observed transuding mRFP-GFP-LC3 adenovirus. effect on gp120-induced cells examined expression p-AKT, p-IKK, p65 nuclei ATG5. promoted MCP-1 IL-17, flux, up-regulated ATG5, while down-regulated phenomena above. Curcumin has similar effects 3-MA, which inhibited NF-κB preventing translocation p65. also phosphorylation p-PI3K, down-regulation NF-κB. reduced via PI3K/AKT/IKK/NF-κB, thereby reducing cellular induced gp120.
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