Evidence map›Paper›PMID 33420900›Full record

ArticleChinese journal of integrative medicine2021

Ginsenoside Rb1 Protects Human Umbilical Vein Endothelial Cells against High Glucose-Induced Mitochondria-Related Apoptosis through Activating SIRT3 Signalling Pathway.

Shi-Ye Ke, Shu-Jie Yu, Ding-Hui Liu, Guang-Yao Shi, Min Wang, Bin Zhou, Lin Wu, Zhi-Ming Song, Jie-Ming Zhu, Chao-Dong Wu and 1 more

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In one paragraph

Article in Chinese journal of integrative medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

4 citing papers in PubMed, 10 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 4 institutions in 2 countries.

Shi-Ye KeDepartment of Cardiology, the Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510630, China.
Shu-Jie YuDepartment of Cardiology, the Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510630, China.
Ding-Hui LiuDepartment of Cardiology, the Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510630, China.
Guang-Yao ShiDepartment of Cardiology, the Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510630, China.
Min WangDepartment of Cardiology, the Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510630, China.
Bin ZhouDepartment of Cardiology, the Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510630, China.
Lin WuDepartment of Cardiology, the Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510630, China.
Zhi-Ming SongDepartment of Cardiology, the First Affiliated Hospital of Henan University, Kaifeng, Henan Province, 475001, China.
Jie-Ming ZhuDepartment of Cardiology, the Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510630, China.
Chao-Dong WuDepartment of Nutrition and Food Science, Texas A&M University, College Station, TX, 77843, United States of America.
Xiao-Xian QianDepartment of Cardiology, the Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510630, China. qianxx@mail.sysu.edu.cn.
Sun Yat-sen University · CNThird Affiliated Hospital of Sun Yat-sen University · CNFirst Affiliated Hospital of Henan University · CNTexas A&M University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate whether ginsenoside Rb1 (Rb1) can protect human umbilical vein endothelial cells (HUVECs) against high glucose-induced apoptosis and examine the underlying mechanism.

methodsHUVECs were divided into 5 groups: control group (5.5 mmol/L glucose), high glucose (HG, 40 mmol/L) treatment group, Rb1 (50 µ mol/L) treatment group, Rb1 plus HG treatment group, and Rb1 and 3-(

resultsRb1 ameliorated survival in cells in which apoptosis was induced by high glucose (P<0.05 or P<0.01). Upon the addition of Rb1, mitochondrial and intracellular reactive oxygen species generation and malondialdehyde levels were decreased (P<0.01), while the activities of antioxidant enzymes were increased (P<0.05 or P<0.01). Rb1 preserved the mitochondrial membrane potential and reduced the release of Cyt-c from the mitochondria into the cytosol (P<0.01). In addition, Rb1 upregulated mitochondrial biogenesis-associated proteins (P<0.01). Notably, the cytoprotective effects of Rb1 were correlated with SIRT3 signalling pathway activation (P<0.01). The effect of Rb1 against high glucose-induced mitochondria-related apoptosis was restrained by 3-TYP (P<0.05 or P<0.01).

conclusionRb1 could protect HUVECs from high glucose-induced apoptosis by promoting mitochondrial function and suppressing oxidative stress through the SIRT3 signalling pathway.

Indexed as

MitochondriaApoptosisEndothelial CellsGinsenosidesGlucoseHumansHuman Umbilical Vein Endothelial CellsReactive Oxygen SpeciesRetinoblastoma Binding ProteinsSirtuin 3Ubiquitin-Protein LigasesUmbilical Cordginsenoside Rb1GinsenosidesGlucoseRB1 protein, humanReactive Oxygen SpeciesRetinoblastoma Binding ProteinsSIRT3 protein, humanSirtuin 3Ubiquitin-Protein Ligasesapoptosisginsenoside Rb1high glucosehuman umbilical vein endothelial cellsmitochondriaSIRT3 signalling pathway

Identifiers

PMID33420900
OpenAlexW3119536340

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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.