Evidence map›Paper›PMID 32088907›Full record

ArticleCell stress & chaperones2020

Berberine attenuates mitochondrial dysfunction by inducing autophagic flux in myocardial hypoxia/reoxygenation injury.

Na Zhu, Xueming Cao, Peiyuan Hao, Yuwei Zhang, Yan Chen, Jing Zhang, Jiang Li, Chuanyu Gao, Li Li

Abstract read
In one paragraph

Article in Cell stress & chaperones, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

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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

9 authors.

Na ZhuDepartment of Health Management, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, Henan University People's Hospital, Zhengzhou, 450003, Henan, People's Republic of China.
Xueming CaoDepartment of Cardiology, Henan Provincial Key Lab For Control of Coronary Heart Disease, Henan Provincial People's Hospital, Central China Fuwai Hospital, Zhengzhou University Central China Fuwai Hospital, Henan University People's Hospital, Zhengzhou, 450003, People's Republic of China.
Peiyuan HaoDepartment of Cardiology, Henan Provincial Key Lab For Control of Coronary Heart Disease, Henan Provincial People's Hospital, Central China Fuwai Hospital, Zhengzhou University Central China Fuwai Hospital, Henan University People's Hospital, Zhengzhou, 450003, People's Republic of China.
Yuwei ZhangMedical Genetic Institute of Henan Province, Henan Provincial People's Hospital, Zhengzhou university people's hospital, Henan University People's Hospital, Zhengzhou, 450003, China.
Yan ChenDepartment of Cardiology, Henan Provincial Key Lab For Control of Coronary Heart Disease, Henan Provincial People's Hospital, Central China Fuwai Hospital, Zhengzhou University Central China Fuwai Hospital, Henan University People's Hospital, Zhengzhou, 450003, People's Republic of China.
Jing ZhangDepartment of Cardiology, Henan Provincial Key Lab For Control of Coronary Heart Disease, Henan Provincial People's Hospital, Central China Fuwai Hospital, Zhengzhou University Central China Fuwai Hospital, Henan University People's Hospital, Zhengzhou, 450003, People's Republic of China.
Jiang LiHenan Provincial Research Center of Natural Medicine Extraction and Medical Technology Application Engineering, Zhengzhou Railway Vocational Technical College, Zhengzhou, 451460, China.
Chuanyu GaoDepartment of Cardiology, Henan Provincial Key Lab For Control of Coronary Heart Disease, Henan Provincial People's Hospital, Central China Fuwai Hospital, Zhengzhou University Central China Fuwai Hospital, Henan University People's Hospital, Zhengzhou, 450003, People's Republic of China. hncxm2007@henu.edu.cn.
Li LiDepartment of Scientific Research and Discipline Construction, Henan Provincial People's Hospital, Zhengzhou university people's hospital, Henan University People's Hospital, Zhengzhou, 450003, China. kxzn2008@henu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Berberine (BBR) is routinely prescribed in many Asian countries to treat diarrhea. Evidence from both animal and clinical investigations suggests that BBR exerts diverse pharmacological activities, including antidiabetic, antineoplastic, antihypertensive, and antiatherosclerotic effects. This study aimed to explore the cardioprotective mechanisms of BBR and to elucidate the modulations between autophagy and mitochondrial function during hypoxia/reoxygenation (H/R) in H9c2 cells. The degree of autophagic flux was assessed by pretreating H9c2 cells with BBR prior to H/R exposure and measuring the expression levels of Beclin-1 and green fluorescent protein (GFP)-labeled LC3B fusion proteins as well as the LC3II/LC3I ratio. The mitochondrial membrane potential (△Ψm) in H9c2 cells was evaluated by detecting rhodamine-123 fluorescence using flow cytometry. The results revealed that pretreatment with BBR upregulated autophagic flux and protected against the loss of the △Ψm in H9c2 cells subjected to H/R. We conclude that BBR attenuates mitochondrial dysfunction by inducing autophagic flux.

Indexed as

AnimalsApoptosisAutophagyBerberineCell DeathCells, CulturedMembrane Potential, MitochondrialMitochondriaMyocardial Reperfusion InjuryMyocytes, CardiacRatsBerberineAutophagic fluxBerberineHypoxia/reoxygenationMitochondrial dysfunction

Identifiers

PMID32088907
PMCPMC7193011

What Socratic 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 Socratic graph.