Evidence map›Paper›PMID 32394311›Full record

ArticleMolecular and cellular biochemistry2020

Astragaloside IV protects human cardiomyocytes from hypoxia/reoxygenation injury by regulating miR-101a.

Yang Wu, Zongjing Fan, Zhengju Chen, Jiqiang Hu, Jie Cui, Yang Liu, Yao Wang, Bin Guo, Juan Shen, Liandi Xie

Open access · hybridAbstract read
In one paragraph

Article in Molecular and cellular biochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

12 citing papers in PubMed, 21 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

10 authors at 1 institution in 1 country.

Yang WuDepartment of CardiologyDong Fang HospitalFengtai District, Beijing University of Chinese Medicine, No. 1 Chang Xin Dian Chen Zhuang Avenue, Beijing, 100078, China.
Zongjing FanDepartment of CardiologyDong Fang HospitalFengtai District, Beijing University of Chinese Medicine, No. 1 Chang Xin Dian Chen Zhuang Avenue, Beijing, 100078, China.
Zhengju ChenTechnical Consultant Department of Technology Center, Beijing 100Biotech Co., Ltd, Beijing, 100078, China.
Jiqiang HuDepartment of CardiologyDong Fang HospitalFengtai District, Beijing University of Chinese Medicine, No. 1 Chang Xin Dian Chen Zhuang Avenue, Beijing, 100078, China.
Jie CuiDepartment of CardiologyDong Fang HospitalFengtai District, Beijing University of Chinese Medicine, No. 1 Chang Xin Dian Chen Zhuang Avenue, Beijing, 100078, China.
Yang LiuDepartment of CardiologyDong Fang HospitalFengtai District, Beijing University of Chinese Medicine, No. 1 Chang Xin Dian Chen Zhuang Avenue, Beijing, 100078, China.
Yao WangBeijing University of Chinese Medicine, Beijing, 100078, China.
Bin GuoBeijing University of Chinese Medicine, Beijing, 100078, China.
Juan ShenDepartment of CardiologyDong Fang HospitalFengtai District, Beijing University of Chinese Medicine, No. 1 Chang Xin Dian Chen Zhuang Avenue, Beijing, 100078, China.
Liandi XieDepartment of CardiologyDong Fang HospitalFengtai District, Beijing University of Chinese Medicine, No. 1 Chang Xin Dian Chen Zhuang Avenue, Beijing, 100078, China. xieliandi74@163.com.ORCID http://orcid.org/0000-0002-4256-8580
Beijing University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Astragaloside IV (AS/IV) is one of the extracted components from the traditional Chinese medicine Astragalus which has been demonstrated to have potential capacity for anti-inflammation activity and for treating cardiovascular disease. Our purpose was to determine the function and underlying molecular mechanism of AS/IV in hypoxia/reoxygenation (H/R) injured in cardiomyocytes. Differentially expressed genes (DEGs) were screened using bioinformatic analysis, and the molecular targeting relationship was verified by the dual-luciferase report system. H/R injured cardiomyocytes were employed to explore the effect of AS/IV. QRT-PCR and Western blot analysis were applied to detect the expression of mRNA and proteins, respectively. Additionally, superoxide dismutase (SOD), lactic dehydrogenase (LDH) and MDA (malondialdehyde) levels were detected to determine the oxidative damage. Cell viability was assessed by CCK-8, and flow cytometry was used to evaluate cell apoptosis ratio. TGFBR1 and TLR2 were selected as DEGs. Additionally, AS/IV could enhance cell proliferation and upregulated miR-101a expression, which suppressed TGFBR1 and TLR2 expression in H/R injured cardiomyocytes. Moreover, the results of Western blot exhibited that the downstream genes (p-ERK and p-p38) in the MAPK signaling pathway were suppressed, which meant AS/IV could inhibit this pathway in H/R injured cardiomyocytes. Overall, this study demonstrated AS/IV could attenuate H/R injury in human cardiomyocytes via the miR-101a/TGFBR1/TLR2/MAPK signaling pathway axis, which means that it could serve as a possible alternate for H/R treatment.

Indexed as

ApoptosisCell HypoxiaCell ProliferationCell SurvivalComputational BiologyGene Expression ProfilingHumansInflammationL-Lactate DehydrogenaseMalondialdehydeMAP Kinase Signaling SystemMicroRNAsMyocardial Reperfusion InjuryMyocytes, CardiacReceptor, Transforming Growth Factor-beta Type IRegenerationastragaloside AL-Lactate DehydrogenaseMalondialdehydeMicroRNAsMIRN101 microRNA, humanReceptor, Transforming Growth Factor-beta Type ISaponinsSuperoxide DismutaseTGFBR1 protein, humanTLR2 protein, humanToll-Like Receptor 2TriterpenesAstragaloside IVHypoxia/reoxygenation injuryMAPK signaling pathwayMiR-101a

Identifiers

PMID32394311
PMCPMC7272390
OpenAlexW3024886008

What Socratic holds

Textmetadata
LicenceCC BY
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.