机构：[1]Department of Pathophysiology, School of Medicine, Jinan University, Guangzhou 510632, Guangdong, China[2]Laboratory of Pathophysiology, State Administration of Traditional Chinese Medicine, School of Medicine, Jinan University, Guangzhou 510632, Guangdong, China[3]GHM Institute of CNS Regeneration, Jinan University, Guangzhou 510632, Guangdong, China[4]Department of Orthopaedics, The First Affiliated Hospital, Jinan University, Guangzhou 510632, Guangdong, China
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, the mechanism of this process remained unclear. Autophagy is a lysosome-mediated cell content-dependent degradation pathway, and uncontrolled autophagy leads to enhanced inflammation. The role of autophagy in curcumin-attenuating BV2 cell inflammation caused by gp120 was investigated with or without pretreatment with the autophagy inhibitor 3-MA and blockers of NF-κB, IKK, AKT, and PI3K, and we then detected the production of the inflammatory mediators monocyte chemoattractant protein-1 (MCP-1) and IL17 using ELISA, and autophagy markers ATG5 and LC3 II by Western Blot. The autophagic flux was observed by transuding mRFP-GFP-LC3 adenovirus. The effect of the blockers on gp120-induced BV2 cells was examined by the expression of p-AKT, p-IKK, NF-κB, and p65 in the nuclei and LC3 II and ATG5. gp120 promoted the expression of MCP-1 and IL-17, enhanced autophagic flux, and up-regulated the expression of LC3 II and ATG5, while the autophagy inhibitor 3-MA down-regulated the phenomena above. Curcumin has similar effects with 3-MA, in which curcumin inhibited NF-κB by preventing the translocation of NF-κB p65. Curcumin also inhibited the phosphorylation of p-PI3K, p-AKT, and p-IKK, which leads to down-regulation of NF-κB. Curcumin reduced autophagy via PI3K/AKT/IKK/NF-κB, thereby reducing BV2 cellular inflammation induced by gp120.
基金：
This work was supported by grants from the
National Natural Science Foundation of China (81171134 and
81471235), Guangdong Provincial Natural Science Foundation of
China (2014A030313360), the Program of Introducing Talents of Discipline
to Universities (B14036), the Science and Technology Foundation
of Guangdong (2010B030700016), and the cultivation and innovation
fund of Jinan University (No. 21617460).
语种：
外文
PubmedID：
中科院(CAS)分区：
出版当年[2017]版：
大类|3 区生物
小类|4 区细胞生物学4 区神经科学
最新[2025]版：
大类|4 区医学
小类|4 区细胞生物学4 区神经科学
第一作者：
第一作者机构：[1]Department of Pathophysiology, School of Medicine, Jinan University, Guangzhou 510632, Guangdong, China[2]Laboratory of Pathophysiology, State Administration of Traditional Chinese Medicine, School of Medicine, Jinan University, Guangzhou 510632, Guangdong, China[3]GHM Institute of CNS Regeneration, Jinan University, Guangzhou 510632, Guangdong, China
共同第一作者：
通讯作者：
通讯机构：[1]Department of Pathophysiology, School of Medicine, Jinan University, Guangzhou 510632, Guangdong, China[2]Laboratory of Pathophysiology, State Administration of Traditional Chinese Medicine, School of Medicine, Jinan University, Guangzhou 510632, Guangdong, China[3]GHM Institute of CNS Regeneration, Jinan University, Guangzhou 510632, Guangdong, China
推荐引用方式(GB/T 7714)：
Guiling Chen,Sisi Liu,Rui Pan,et al.Curcumin Attenuates gp120-Induced Microglial Inflammation by Inhibiting Autophagy via the PI3K Pathway.[J].Cellular and molecular neurobiology.2018,38(8):1465-1477.doi:10.1007/s10571-018-0616-3.
APA：
Guiling Chen,Sisi Liu,Rui Pan,Guangming Li,Haijie Tang...&Jun Dong.(2018).Curcumin Attenuates gp120-Induced Microglial Inflammation by Inhibiting Autophagy via the PI3K Pathway..Cellular and molecular neurobiology,38,(8)
MLA：
Guiling Chen,et al."Curcumin Attenuates gp120-Induced Microglial Inflammation by Inhibiting Autophagy via the PI3K Pathway.".Cellular and molecular neurobiology 38..8(2018):1465-1477
