Evidence map›Paper›PMID 31221142›Full record

ArticleBMC complementary and alternative medicine2019

ERK/Nrf2 pathway activation by caffeic acid in HepG2 cells alleviates its hepatocellular damage caused by t-butylhydroperoxide-induced oxidative stress.

Sung-Yong Yang, Min Cheol Pyo, Mi-Hyun Nam, Kwang-Won Lee

Open access · goldAbstract read
In one paragraph

Article in BMC complementary and alternative medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.4field-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

35 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Review
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  6. Review
  7. Carboxylic Acids as Activators of NRF2: Antioxidant and Anti-inflammatory Effects.Medicinal chemistry (Shariqah (United Arab Emirates)) · 2025
    Review
  8. Physiology and molecular biology of plants : an international journal of functional plant biology · 2024
    Review
  9. Adjuvant Properties of Caffeic Acid in Cancer Treatment.International journal of molecular sciences · 2024
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Potential ofMolecules (Basel, Switzerland) · 2022
    Review
  19. Article
  20. Review
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

4 authors at 2 institutions in 2 countries.

Sung-Yong Yang212 CJ Food Safety Hall, Institute of Life Science and Natural Resources, Korea University, Anam-Dong, Sungbuk-Gu, Seoul, 02841, South Korea.
Min Cheol PyoDepartment of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, 02841, South Korea.
Mi-Hyun NamDepartment of Ophthalmology, University of Colorado School of Medicine, Aurora, CO, 80045, USA.
Kwang-Won LeeDepartment of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, 02841, South Korea. kwangwon@korea.ac.kr.ORCID http://orcid.org/0000-0001-5326-469X
Korea University · KRUniversity of Colorado Denver · US

Funding

Korea University Grant K1617111National Research Foundation of Korea grant 2017R1A2B412182
6 · The paper itself

Abstract

backgroundSeveral studies have found that caffeic acid (CA), a well-known phytochemical, displays important antioxidant and anti-cancer activities. However, no evidence exists on the protective effect and its mechanisms that CA treatment alone has against oxidative stress induced by tert-butyl hydroperoxide (t-BHP) in HepG2 cells.

methodsHepatoprotective activities such as cell viability, mRNA expression, and report gene assay were measured using HepG2 cell. Three types of genes and proteins related with detoxification in liver were used for measuring the hepatoprotective effects. Statistical analysis was performed using one-way ANOVA test and differences among groups were evaluated by Tukey's studentized range tests.

resultsThe present study indicate that treatment with CA up-regulates heme oxygenase-1 (HO-1) and glutamate-cysteine ligase (GCL) mRNA and protein expressions in a CA-dose-dependent manner. In addition, translocation of nuclear factor-E2 p45-related factor (Nrf2) from the cytoplasm to the nucleus and phosphorylation of extracellular signal-regulated kinase, ERK and c-Jun N-terminal kinase, JNK which have been shown to be involved in mitogen-activated protein kinases, MAPKs are significantly enhanced by CA treatment. Furthermore, in cell nuclei, CA enhances the 5'-flanking regulatory region of human antioxidant response element (ARE) and activates the ARE binding site.

conclusionTherefore, CA proved to be a stimulant of the expression of detoxification enzymes such as HO-1, GCLC, and GCLM through the ERK/Nrf2 pathway, and it may be an effective chemoprotective agent for protecting liver damage against oxidative damage.

Indexed as

Antioxidant Response ElementsCaffeic AcidsCell SurvivalExtracellular Signal-Regulated MAP KinasesGlutamate-Cysteine LigaseHeme Oxygenase-1Hep G2 CellsHumansJNK Mitogen-Activated Protein KinasesLiverLiver NeoplasmsNF-E2-Related Factor 2Oxidative StressProtective AgentsReactive Oxygen Speciestert-ButylhydroperoxideCaffeic AcidsExtracellular Signal-Regulated MAP KinasesGlutamate-Cysteine LigaseHeme Oxygenase-1JNK Mitogen-Activated Protein KinasesNF-E2-Related Factor 2Protective AgentsReactive Oxygen Speciestert-ButylhydroperoxideAntioxidant response elementCaffeic acidERK/Nrf2 pathwayGlutamate-cysteine ligasetert-butyl hydroperoxide

Identifiers

PMID31221142
PMCPMC6585055
OpenAlexW2949417693

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.