Evidence map›Paper›PMID 30088211›Full record

ArticleChinese journal of integrative medicine2019

Ginsenoside Rb1 Ameliorates Autophagy of Hypoxia Cardiomyocytes from Neonatal Rats via AMP-Activated Protein Kinase Pathway.

Sheng-Nan Dai, Ai-Jie Hou, Shu-Mei Zhao, Xiao-Ming Chen, Hua-Ting Huang, Bo-Han Chen, Hong-Liang Kong

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Article in Chinese journal of integrative medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

9 citing papers in PubMed, 18 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

7 authors at 4 institutions in 1 country.

Sheng-Nan DaiDepartment of Cardiology, the People's Hospital of China Medical University, the People's Hospital of Liaoning Province, Shenyang, 110016, China.
Ai-Jie HouDepartment of Cardiology, the People's Hospital of China Medical University, the People's Hospital of Liaoning Province, Shenyang, 110016, China.
Shu-Mei ZhaoInternational Education College, Shenyang Normal University, Shenyang, 110034, China.
Xiao-Ming ChenDepartment of Cardiology, the People's Hospital of China Medical University, the People's Hospital of Liaoning Province, Shenyang, 110016, China.
Hua-Ting HuangDepartment of Cardiology, the People's Hospital of China Medical University, the People's Hospital of Liaoning Province, Shenyang, 110016, China.
Bo-Han ChenDepartment of Cardiology, the First Affiliated Hospital of Dalian Medical University, Dalian, 116044, China.
Hong-Liang KongDepartment of Cardiology, the People's Hospital of China Medical University, the People's Hospital of Liaoning Province, Shenyang, 110016, China. khl339@163.com.
China Medical University · CNLiaoning Provincial People's Hospital · CNFirst Affiliated Hospital of Dalian Medical University · CNShenyang Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate whether ginsenoside-Rb1 (Gs-Rb1) improves the CoCl-induced autophagy of cardiomyocytes via upregulation of adenosine 5'-monophosphate-activated protein kinase (AMPK) pathway.

methodsVentricles from 1- to 3-day-old Wistar rats were sequentially digested, separated and incubated in Dulbecco's modified Eagle's medium supplemented with 10% fetal bovine serum for 3 days followed by synchronization. Neonatal rat cardiomyocytes were randomly divided into 7 groups: control group (normal level oxygen), hypoxia group (500 μmol/L CoCl

resultsGs-Rb1 significantly improved the cell viability of hypoxia cardiomyocytes (P<0.01). However, the viability of hypoxia-treated cardiomyocytes was significantly inhibited by Ara A (P<0.01). Gs-Rb1 increased the AMPK activity of hypoxia-treated cardiomyocytes. The AMPK activity of hypoxia-treated cadiomyocytes was inhibited by Ara A (P<0.01) and was not affected by AICAR =0.983). Gs-Rb1 up-regulated Atg4B, Atg5, Beclin-1, Atg7, LC3B II, the LC3B II/I ratio and cathepsin B activity of hypoxia cardiomyocytes (P<0.05), each of these protein levels was significantly enhanced by Ara A (all P<0.01), but was not affected by AICAR (all P>0.05). Gs-Rb1 significantly down-regulated P62 levels of hypoxic cardiomyocytes (P<0.05). The P62 levels of hypoxic cardiomyocytes were inhibited by Ara A (P<0.05) and were not affected by AICAR (P=0.871).

conclusionGs-Rb1 may improve the viability of hypoxia cardiomyocytes by ameliorating cell autophagy via the upregulation of AMPK pathway.

Indexed as

AMP-Activated Protein KinasesAnimalsAnimals, NewbornAutophagyBiomarkersCathepsin BCell HypoxiaCell SurvivalGinsenosidesLysosomesMyocytes, CardiacRats, WistarSequestosome-1 ProteinSignal TransductionTroponin IAMP-Activated Protein KinasesBiomarkersCathepsin Bginsenoside Rb1GinsenosidesSequestosome-1 ProteinSqstm1 protein, ratTroponin Iadenosine 5′-monophosphate-activated protein kinaseautophagic fluxcardiomyocytesginsenosides-Rb1hypoxia

Identifiers

PMID30088211
OpenAlexW2886770714

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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.