Evidence map›Paper›PMID 27980220›Full record

ArticleOncotarget2017

Berberine augments ATP-induced inflammasome activation in macrophages by enhancing AMPK signaling.

Chen-Guang Li, Liang Yan, Yan-Yun Jing, Li-Hui Xu, Yi-Dan Liang, Hong-Xia Wei, Bo Hu, Hao Pan, Qing-Bing Zha, Dong-Yun Ouyang and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
5.2field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 40 citations in OpenAlex.

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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

11 authors at 2 institutions in 1 country.

Chen-Guang LiDepartment of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou, China.
Liang YanDepartment of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou, China.
Yan-Yun JingDepartment of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou, China.
Li-Hui XuDepartment of Cell Biology, College of Life Science and Technology, Jinan University, Guangzhou, China.
Yi-Dan LiangDepartment of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou, China.
Hong-Xia WeiDepartment of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou, China.
Bo HuDepartment of Nephrology, the First Affiliated Hospital of Jinan University, Guangzhou, China.
Hao PanDepartment of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou, China.
Qing-Bing ZhaDepartment of Fetal Medicine, the First Affiliated Hospital of Jinan University, Guangzhou, China.
Dong-Yun OuyangDepartment of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou, China.
Xian-Hui HeDepartment of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou, China.
Jinan University · CNFirst Affiliated Hospital of Jinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The isoquinoline alkaloid berberine possesses many pharmacological activities including antibacterial infection. Although the direct bactericidal effect of berberine has been documented, its influence on the antibacterial functions of macrophages is largely unknown. As inflammasome activation in macrophages is important for the defense against bacterial infection, we aimed to investigate the influence of berberine on inflammasome activation in murine macrophages. Our results showed that berberine significantly increased ATP-induced inflammasome activation as reflected by enhanced pyroptosis as well as increased release of caspase-1p10 and mature interleukin-1β (IL-1β) in macrophages. Such effects of berberine could be suppressed by AMP-activated protein kinase (AMPK) inhibitor compound C or by knockdown of AMPKα expression, indicating the involvement of AMPK signaling in this process. In line with increased IL-1β release, the ability of macrophages to kill engulfed bacteria was also intensified by berberine. This was corroborated by the in vivo finding that the peritoneal live bacterial load was decreased by berberine treatment. Moreover, berberine administration significantly improved survival of bacterial infected mice, concomitant with increased IL-1β levels and elevated neutrophil recruitment in the peritoneal cavity. Collectively, these data suggested that berberine could enhance bacterial killing by augmenting inflammasome activation in macrophages through AMPK signaling.

Indexed as

Adenosine TriphosphateAnimalsBacterial InfectionsBerberineFemaleInflammasomesMacrophagesMacrophages, PeritonealMAP Kinase Signaling SystemMiceMicrobial ViabilityNeutrophil InfiltrationNeutrophilsAdenosine TriphosphateBerberineInflammasomesAMP-activated protein kinase (AMPK)antibacterial infectionberberineImmune responseImmunityImmunology and Microbiology Sectioninflammasomemacrophages

Identifiers

PMID27980220
PMCPMC5352208
OpenAlexW2564290392

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.