Evidence map›Paper›PMID 26539255›Full record

ArticleOxidative medicine and cellular longevity2015

EGCG Attenuates Uric Acid-Induced Inflammatory and Oxidative Stress Responses by Medicating the NOTCH Pathway.

Hua Xie, Jianqin Sun, Yanqiu Chen, Min Zong, Shijie Li, Yan Wang

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Review
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  7. Review
  8. Article
  9. Biological Effects of EGCG@MOF Zn(BTC)Molecules (Basel, Switzerland) · 2022
    Article
  10. Article
  11. Hyperuricemia-induced endothelial insulin resistance: the nitric oxide connection.Pflugers Archiv : European journal of physiology · 2022
    Review
  12. Anti-Inflammatory Effects ofJournal of inflammation research · 2022
    Article
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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

6 authors at 2 institutions in 1 country.

Hua XieNutrition Department, Huadong Hospital Affiliated to Fudan University, Shanghai 200040, China.
Jianqin SunNutrition Department, Huadong Hospital Affiliated to Fudan University, Shanghai 200040, China.
Yanqiu ChenNutrition Department, Huadong Hospital Affiliated to Fudan University, Shanghai 200040, China.
Min ZongNutrition Department, Huadong Hospital Affiliated to Fudan University, Shanghai 200040, China.
Shijie LiNutrition Department, Huadong Hospital Affiliated to Fudan University, Shanghai 200040, China.
Yan WangNutrition Department, Huadong Hospital Affiliated to Fudan University, Shanghai 200040, China.
Huadong Hospital · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe aim of this study is to investigate whether (-)-epigallocatechin-3-gallate (EGCG) can prevent the UA-induced inflammatory effect of human umbilical vein endothelial cells (HUVEC) and the involved mechanisms in vitro.

methodsHUVEC were subjected to uric acid (UA) with or without EGCG treatment. RT-PCR and western blots were performed to determine the level of inflammation marker. The antioxidant activity was evaluated by measuring scavenged reactive oxygen species (ROS). Functional studies of the role of Notch-1 in HUVEC lines were performed using RNA interference analyses.

resultsUA significantly increased the expressions of IL-6, ICAM-1, TNF-α, and MCP-1 and the production of ROS in HUVEC. Meanwhile, the expression of Notch-1 and its downstream effects significantly increased. Using siRNA, inhibition of Notch-1 signaling significantly impeded the expressions of inflammatory cytokines under UA treatment. Interestingly, EGCG suppressed the expressions of inflammatory cytokines and the generation of ROS. Western blot analysis of Notch-1 showed that EGCG significantly decreased the expressions of inflammatory cytokines through Notch-1 signaling pathways.

conclusionsIn summary, our findings indicated that Notch-1 plays an important role in the UA-induced inflammatory response, and the downregulation of Notch-1 by EGCG could be an effective approach to decrease inflammation and oxidative stress induced by UA.

Indexed as

CatechinChemokine CCL2Down-RegulationHumansHuman Umbilical Vein Endothelial CellsIntercellular Adhesion Molecule-1Interleukin-6Oxidative StressReactive Oxygen SpeciesReal-Time Polymerase Chain ReactionReceptors, NotchRNA InterferenceRNA, Small InterferingSignal TransductionTumor Necrosis Factor-alphaUp-RegulationCatechinCCL2 protein, humanChemokine CCL2epigallocatechin gallateIntercellular Adhesion Molecule-1Interleukin-6Reactive Oxygen SpeciesReceptors, NotchRNA, Small InterferingTumor Necrosis Factor-alphaUric Acid

Identifiers

PMID26539255
PMCPMC4619967
OpenAlexW1955449518

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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.