Evidence map›Paper›PMID 32401923›Full record

ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2020

Notoginsenoside R1 upregulates miR-221-3p expression to alleviate ox-LDL-induced apoptosis, inflammation, and oxidative stress by inhibiting the TLR4/NF-κB pathway in HUVECs.

Lingbo Zhu, Xinyan Gong, Jianping Gong, Yungang Xuan, Ting Fu, Shimao Ni, Lei Xu, Ningning Ji

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
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  10. Microbiology spectrum · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Lingbo ZhuDepartment of Cardiology, Central Hospital of Yiwu, Yiwu, Zhejiang, China.
Xinyan GongDepartment of Cardiology, Central Hospital of Yiwu, Yiwu, Zhejiang, China.
Jianping GongDepartment of Cardiology, Central Hospital of Yiwu, Yiwu, Zhejiang, China.
Yungang XuanDepartment of Cardiology, Central Hospital of Yiwu, Yiwu, Zhejiang, China.
Ting FuDepartment of Cardiology, Central Hospital of Yiwu, Yiwu, Zhejiang, China.
Shimao NiDepartment of Cardiology, Central Hospital of Yiwu, Yiwu, Zhejiang, China.
Lei XuDepartment of Cardiology, Central Hospital of Yiwu, Yiwu, Zhejiang, China.
Ningning JiDepartment of Cardiology, Central Hospital of Yiwu, Yiwu, Zhejiang, China.
Yichang Central People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis (AS) is a common vascular disease, which can cause apoptosis of vascular endothelial cells. Notoginsenoside R1 (NGR1) is considered an anti-AS drug. MicroRNAs (miRNAs) are believed to play a vital role in cell apoptosis and angiogenesis. This study aimed to explore the mechanism of NGR1 for treating AS through miRNAs. Flow cytometry was used to detect the apoptosis rate. The levels of inflammatory cytokines interleukin (IL)-6 and IL-1β were detected using ELISA. Reactive oxygen species (ROS) and malondialdehyde (MDA) levels were measured using corresponding assay kits. Quantitative real-time polymerase chain reaction (qRT-PCR) assay was performed to detect miR-221-3p expression. Dual-luciferase reporter and RNA immunoprecipitation assays were carried out to examine the relationship between miR-221-3p and toll-like receptors 4 (TLR4). Also, western blot analysis was performed to determine the levels of TLR4 and nuclear factor kappa B (NF-κB) signaling pathway-related proteins. Oxidized low-density lipoprotein (ox-LDL) induced human umbilical vein endothelial cells (HUVECs) apoptosis, inflammation, and oxidative stress. NGR1 alleviated the negative effect of ox-LDL through promoting the expression of miR-221-3p in HUVECs. TLR4 was a target of miR-221-3p, and its overexpression could reverse the inhibition effects of miR-221-3p on apoptosis, inflammation, and oxidative stress. NGR1 improved miR-221-3p expression to inhibit the activation of the TLR4/NF-κB pathway in ox-LDL-treated HUVECs. NGR1 decreased ox-LDL-induced HUVECs apoptosis, inflammation, and oxidative stress through increasing miR-221-3p expression, thereby inhibiting the activation of the TLR4/NF-κB pathway. This study of the mechanism of NGR1 provided a more theoretical basis for the treatment of AS.

Indexed as

ApoptosisBlotting, WesternEnzyme-Linked Immunosorbent AssayGinsenosidesHumansHuman Umbilical Vein Endothelial CellsImmunoprecipitationInflammationLipoproteins, LDLMicroRNAsNF-kappa BOxidative StressReactive Oxygen SpeciesReal-Time Polymerase Chain ReactionSignal TransductionToll-Like Receptor 4GinsenosidesLipoproteins, LDLMicroRNAsMIR221, humanNF-kappa Bnotoginsenoside R1oxidized low density lipoproteinReactive Oxygen SpeciesTLR4 protein, humanToll-Like Receptor 4

Identifiers

PMID32401923
PMCPMC7233198
OpenAlexW3024798471

What OpenQuestion holds

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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 OpenQuestion graph.