Evidence map›Paper›PMID 30402951›Full record

Trial reportPhytotherapy research : PTR2019

Berberine alleviates oxidized low-density lipoprotein-induced macrophage activation by downregulating galectin-3 via the NF-κB and AMPK signaling pathways.

ChongZhe Pei, Yi Zhang, Ping Wang, BeiJian Zhang, Lu Fang, Bo Liu, Shu Meng

Open access · hybridAbstract readRandomized Controlled Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Phytotherapy research : PTR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 3 pooled it
2.0field-weighted citation impact, top 13% 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

34 citing papers in PubMed, 3 syntheses or guidelines pooled it, 78 citations in OpenAlex.

  1. Review of OxLDL Driven Inflammatory Cell Activation.Current atherosclerosis reports · 2025
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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

7 authors at 2 institutions in 2 countries.

ChongZhe PeiDepartment of Cardiology, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
Yi ZhangDepartment of Cardiology, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
Ping WangDepartment of Laboratory Medicine, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
BeiJian ZhangDepartment of Cardiology, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
Lu FangHaematopoiesis and Leukocyte Biology Laboratory, Baker Heart and Diabetes Research Institute, Melbourne, Victoria, Australia.
Bo LiuDepartment of Cardiology, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
Shu MengDepartment of Cardiology, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.ORCID http://orcid.org/0000-0002-0653-2644
XinHua Hospital · CNBaker Heart and Diabetes Institute · AU

Funding

National Natural Science Foundation of China 81270207Science and Technology Commission of Shanghai Municipality 16401972000
6 · The paper itself

Abstract

Macrophage activation plays a central role in neoatherosclerosis and in-stent restenosis after percutaneous coronary intervention (PCI). Galectin-3, mainly expressed on macrophages, is an important regulator of inflammation. This study aimed to investigate the effects of berberine (BBR) on oxidized low-density lipoprotein (ox-LDL)-induced macrophage activation and galectin-3 expression and their underlying mechanisms. THP-1-derived macrophages were pretreated with BBR prior to stimulation with ox-LDL. Galectin-3 expression was measured by real-time PCR, Western blotting, and confocal microscopy. Macrophage activation was assessed by lipid accumulation, expression of inflammatory cytokines, and CD11b and CD86. Plasma galectin-3 levels were measured in patients undergoing PCI at baseline and after BBR treatment for 3 months. BBR suppressed ox-LDL-induced upregulation of galectin-3 and macrophage activation. Overexpression of galectin-3 intervened the inhibitory effect of BBR on macrophage activation. BBR activated phospho-AMPK and inhibited phospho-NF-κB p65 nuclear translocation. AMPK inhibition and NF-κB activation abolished the inhibitory effects of BBR on galectin-3 expression and macrophage activation. Combination of BBR and rosuvastatin exerted greater effects than BBR or rosuvastatin alone. However, BBR treatment did not further reduce plasma galectin-3 after PCI in patients receiving standard therapy. In conclusion, BBR alleviates ox-LDL-induced macrophage activation by downregulating galectin-3 via the NF-κB and AMPK signaling pathways.

Indexed as

Lipoproteins, LDLAgedAged, 80 and overAMP-Activated Protein KinasesBerberineCells, CulturedDown-RegulationFemaleGalectin 3Gene Expression RegulationHumansInflammationMacrophage ActivationMacrophagesMaleMiddle AgedAMP-Activated Protein KinasesBerberineGalectin 3Lipoproteins, LDLNF-kappa Boxidized low density lipoproteinTranscription Factor RelAberberinegalectin-3macrophage activationrosuvastatin

Identifiers

PMID30402951
PMCPMC6587449
OpenAlexW2899951482

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.