Evidence map›Paper›PMID 25875041›Full record

ArticleMolecules (Basel, Switzerland)2015

Epigallocatechin-3-gallate protects HUVECs from PM2.5-induced oxidative stress injury by activating critical antioxidant pathways.

Guang-Zhao Yang, Zhao-Jun Wang, Feng Bai, Xiao-Jiang Qin, Jing Cao, Ji-Yuan Lv, Ming-Sheng Zhang

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

34 citing papers in PubMed, 79 citations in OpenAlex.

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  11. Djulis (Molecules (Basel, Switzerland) · 2021
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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 1 institution in 1 country.

Guang-Zhao YangThe Fist Clinical Hospital, Shanxi Medical University, 56 Xinjiannanlu, Taiyuan, Shanxi 030001, China. ygzloveqq@126.com.
Zhao-Jun WangDepartment of Pharmacology, Shanxi Medical University, 56 Xinjiannanlu, Taiyuan, Shanxi 030001, China. wzhaojun1025@126.com.
Feng BaiThe Fist Clinical Hospital, Shanxi Medical University, 56 Xinjiannanlu, Taiyuan, Shanxi 030001, China. pinkbai@163.com.
Xiao-Jiang QinDepartment of Pharmacology, Shanxi Medical University, 56 Xinjiannanlu, Taiyuan, Shanxi 030001, China. sxykdxyxy@163.com.
Jing CaoThe Fist Clinical Hospital, Shanxi Medical University, 56 Xinjiannanlu, Taiyuan, Shanxi 030001, China. 13834691242@163.com.
Ji-Yuan LvThe Fist Clinical Hospital, Shanxi Medical University, 56 Xinjiannanlu, Taiyuan, Shanxi 030001, China. lvjiyuan11@163.com.
Ming-Sheng ZhangDepartment of Pharmacology, Shanxi Medical University, 56 Xinjiannanlu, Taiyuan, Shanxi 030001, China. zmspharmacol@sohu.com.
Shanxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial dysfunction and oxidative stress likely play roles in PM2.5-induced harmful effects. Epigallocatechin-3-gallate (EGCG), the major polyphenolic constituent of green tea, is a potent antioxidant that exerts protective effects on cardiovascular diseases (CVDs) in part by scavenging free radicals. The exposure to ambient fine particulate matter (PM2.5) is responsible for certain CVDs. The aim of the present study was to investigate whether EGCG could also inhibit PM2.5-induced oxidative stress by activating the nuclear factor E2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway in human umbilical vein endothelial cells (HUVECs). PM2.5 (200 μg/mL) increased both cell death and intracellular ROS levels significantly, whereas EGCG (50-400 μM) inhibited these effects in a concentration-dependent manner. Western blotting and PCR demonstrated that EGCG increased Nrf2 and HO-1 expression in HUVECs that had been exposed to PM2.5. PD98059 (a selective inhibitor of extracellular signal regulated kinase [ERK]-1/2) and SB203580 (a selective inhibitor of p38 MAPK), but not SP600125 (a selective inhibitor of c-jun N-terminal kinase [JNK]), attenuated the EGCG-induced Nrf2 and HO-1 expression. In addition, silencing Nrf2 abolished EGCG-induced Nrf2 and HO-1 upregulation and enhancement of cell viability. The present study suggests that EGCG protects HUVECs from PM2.5-induced oxidative stress injury by upregulating Nrf2/HO-1 via activation of the p38 MAPK and the ERK1/2 signaling pathways.

Indexed as

AntioxidantsCatechinCell SurvivalGene Expression RegulationGene SilencingHeme Oxygenase-1HumansHuman Umbilical Vein Endothelial CellsInhibitory Concentration 50MAP Kinase Signaling SystemMolecular StructureNF-E2-Related Factor 2Oxidative Stressp38 Mitogen-Activated Protein KinasesParticulate MatterReactive Oxygen SpeciesAntioxidantsCatechinepigallocatechin gallateHeme Oxygenase-1NF-E2-Related Factor 2p38 Mitogen-Activated Protein KinasesParticulate MatterReactive Oxygen Species

Identifiers

PMID25875041
PMCPMC6272777
OpenAlexW1972775556

What OpenQuestion 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 OpenQuestion graph.