Evidence map›Paper›PMID 31993073›Full record

ArticleChinese medicine2020

13-Methylberberine improves endothelial dysfunction by inhibiting NLRP3 inflammasome activation via autophagy induction in human umbilical vein endothelial cells.

Zhihua Peng, Hong Zhan, Yijia Shao, Yan Xiong, Lijin Zeng, Cong Zhang, Zhihao Liu, Zhenhua Huang, Huanxing Su, Zhen Yang

Open access · goldAbstract read
In one paragraph

Article in Chinese medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 4 pooled it
2.0field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 4 syntheses or guidelines pooled it, 29 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

10 authors at 3 institutions in 2 countries.

Zhihua Peng *1Division of Emergency Medicine, Department of Emergency Intensive Care Unit, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080 China.
Hong Zhan *1Division of Emergency Medicine, Department of Emergency Intensive Care Unit, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080 China.
Yijia Shao2Department of Cardiology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080 Guangdong China.
Yan Xiong1Division of Emergency Medicine, Department of Emergency Intensive Care Unit, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080 China.
Lijin Zeng1Division of Emergency Medicine, Department of Emergency Intensive Care Unit, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080 China.
Cong Zhang1Division of Emergency Medicine, Department of Emergency Intensive Care Unit, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080 China.
Zhihao Liu1Division of Emergency Medicine, Department of Emergency Intensive Care Unit, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080 China.
Zhenhua Huang1Division of Emergency Medicine, Department of Emergency Intensive Care Unit, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080 China.
Huanxing SuState Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.
Zhen Yang1Division of Emergency Medicine, Department of Emergency Intensive Care Unit, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080 China.
Sun Yat-sen University · CNThe First Affiliated Hospital, Sun Yat-sen University · CNUniversity of Macau · MO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAtherosclerosis, the underlying cause of the majority of cardiovascular diseases, is a lipid-driven, inflammatory disease of the large arteries. Atherosclerotic cardiovascular disease (ASCVD) threatens human lives due to high morbidity and mortality. Many studies have demonstrated that atherosclerosis is accelerated via activation of the NLRP3 inflammasome. The NLRP3 inflammasome plays a critical role in the development of vascular inflammation and atherosclerosis. In atherosclerotic plaques, excessive generation of reactive oxygen species (ROS) activates the NLRP3 inflammasome. 13-Methylberberine (13-MB) is a newly synthesized compound used in traditional Chinese medicine that has outstanding antibacterial, antitumor, and antiobesity activities, especially anti-inflammatory activity. However, the role of 13-MB in atherosclerosis needs to be explored.

methodsCCK-8 assays and flow cytometry were conducted to determine the cell viability and apoptotic profiles of human umbilical vein endothelial cells (HUVECs) treated with 13-MB. Carboxy-DCFH-DA and JC-10 assays were used to measure ROS and determine mitochondrial membrane potential. Western blot analysis was performed to investigate proteins that are associated with the NLRP3 inflammasome and autophagy. ELISA was used to detect and quantify inflammatory cytokines related to the NLRP3 inflammasome. Transfection and confocal microscopy were conducted to observe autophagy.

resultsPretreatment with 13-MB markedly reduced cytotoxicity and apoptosis, as well as intracellular ROS production, in H

conclusion13-MB exerts cytoprotective effects in an H

Indexed as

13-MethylberberineAnti-inflammatoryAtherosclerosisAutophagy inducerNLRP3 inflammasome

Identifiers

PMID31993073
PMCPMC6977264
OpenAlexW3013970535

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.