Evidence map›Paper›PMID 30106101›Full record

ArticleMolecular medicine reports2018

Oleanolic acid protects against oxidative stress‑induced human umbilical vein endothelial cell injury by activating AKT/eNOS signaling.

Wei Zhang, Jian Feng, Biao Cheng, Qing Lu, Xiaoping Chen

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

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  14. Protective Effects of Water Extract ofVeterinary sciences · 2021
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  15. BioMed research international · 2021
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  16. Review
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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

5 authors at 3 institutions in 1 country.

Wei ZhangDepartment of Geriatric Cardiovascular Medicine, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu, Sichuan 610072, P.R. China.
Jian FengDepartment of Cardiovascular Medicine, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Biao ChengDepartment of Geriatric Cardiovascular Medicine, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu, Sichuan 610072, P.R. China.
Qing LuDepartment of Geriatric Cardiovascular Medicine, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu, Sichuan 610072, P.R. China.
Xiaoping ChenDepartment of Cardiovascular Medicine, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital · CNAffiliated Hospital of Southwest Medical University · CNWest China Hospital of Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative injury of vascular endothelial cells in the initial event of atherosclerosis (AS) in diabetes was assessed in the present study. The antioxidant effect of oleanolic acid (OA) has attracted much attention. In the present study the potential effects of OA on human umbilical vein endothelial cells (HUVECs) were investigated. Cell viability was examined using the CCK‑8 assay. The activity of oxidative stress parameters was determined using commercial kits. Flow cytometry analysis was performed to detect the level of reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and cell apoptosis. The expression levels of target genes and proteins were examined by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blot analysis. It was indicated that cell viability that was suppressed by high glucose was increased by the pretreatment of OA, and nitric oxide (NO) generation, the activities of superoxide dismutase (SOD) and catalase (CAT) were recovered by OA. By contrast, it was observed that OA decreased the MDA content. Notably, the pretreatment of OA alleviated mitochondria damage by reducing the level of ROS and maintaining MMP. In addition, apoptosis that was caused by high glucose was reduced by OA. Pro‑apoptotic genes (caspase‑3, Fas, Fasl) and anti‑apoptotic gene (Bcl‑2) expression levels were decreased and increased in the OA groups, respectively. Furthermore, the activity of AKT/endothelial nitric oxide synthase (eNOS) signaling was elevated by OA. Taken together, it was suggested that OA could protect against oxidative stress‑induced apoptosis of HUVECs, which was associated with AKT/eNOS signaling pathway.

Indexed as

AntioxidantsApoptosisEndothelial CellsHumansHuman Umbilical Vein Endothelial CellsMembrane Potential, MitochondrialNitric Oxide Synthase Type IIIOleanolic AcidOxidative StressProto-Oncogene Proteins c-aktReactive Oxygen SpeciesAntioxidantsNitric Oxide Synthase Type IIINOS3 protein, humanOleanolic AcidProto-Oncogene Proteins c-aktReactive Oxygen Species

Identifiers

PMID30106101
PMCPMC6131357
OpenAlexW2885846237

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.