Evidence map›Paper›PMID 30155758›Full record

ArticleCellular and molecular neurobiology2018

Curcumin Attenuates gp120-Induced Microglial Inflammation by Inhibiting Autophagy via the PI3K Pathway.

Guiling Chen, Sisi Liu, Rui Pan, Guangming Li, Haijie Tang, Mingliang Jiang, Yanyan Xing, Fujun Jin, Liqing Lin, Jun Dong

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.2field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 38 citations in OpenAlex.

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  19. Effects of Curcumin on Microglial Cells.Neurotoxicity research · 2019
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Guiling ChenDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, 510632, Guangdong, China.
Sisi LiuDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, 510632, Guangdong, China.
Rui PanDepartment of Orthopaedics, The First Affiliated Hospital, Jinan University, Guangzhou, 510632, Guangdong, China.
Guangming LiDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, 510632, Guangdong, China.
Haijie TangDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, 510632, Guangdong, China.
Mingliang JiangDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, 510632, Guangdong, China.
Yanyan XingDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, 510632, Guangdong, China.
Fujun JinDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, 510632, Guangdong, China.
Liqing LinDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, 510632, Guangdong, China.
Jun DongDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, 510632, Guangdong, China. dongjunbox@163.com.
State Administration of Traditional Chinese Medicine of the People's Republic of China · CNJinan University · CNFirst Affiliated Hospital of Jinan University · CN

Funding

Guangdong Provincial Natural Science Foundation of China 2014A030313360the cultivation and innovation fund of Jinan University No.21617460the National Natural Science Foundation of China 81171134the National Natural Science Foundation of China 81471235the Program of Introducing Talents of Discipline to Universities B14036the Science and Technology Foundation of Guangdong 2010B030700016
6 · The paper itself

Abstract

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.

Indexed as

Signal TransductionAnimalsAutophagosomesAutophagyChemokine CCL2CurcuminHIV Envelope Protein gp120I-kappa B ProteinsInflammationInterleukin-17MiceMicrogliaNF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktChemokine CCL2CurcuminHIV Envelope Protein gp120I-kappa B ProteinsInterleukin-17NF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAutophagyCurcumingp120InflammationMicrogliaPI3K

Identifiers

PMID30155758
PMCPMC11469807
OpenAlexW2889290617

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.