Evidence map›Paper›PMID 32326032›Full record

ArticleAntioxidants (Basel, Switzerland)2020

Protection against Ultraviolet A-Induced Skin Apoptosis and Carcinogenesis through the Oxidative Stress Reduction Effects of

Yueh-Hsiung Kuo, Hung-Lung Chiang, Po-Yuan Wu, Yin Chu, Qiao-Xin Chang, Kuo-Ching Wen, Chien-Yih Lin, Hsiu-Mei Chiang

Open access · goldAbstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

6 citing papers in PubMed, 18 citations in OpenAlex.

  1. Djulis (Molecules (Basel, Switzerland) · 2025
    Review
  2. International journal of molecular sciences · 2023
    Article
  3. Review
  4. Protective Effect of Djulis (Molecules (Basel, Switzerland) · 2022
    Article
  5. Article
  6. Antioxidants and Skin Protection.Antioxidants (Basel, Switzerland) · 2020
    Article
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

8 authors at 2 institutions in 1 country.

Yueh-Hsiung KuoDepartment of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, China Medical University, Taichung 40402, Taiwan.ORCID 0000-0001-5935-6755
Hung-Lung ChiangDepartment and Graduate School of Safety Health and Environmental Engineering, National Yulin University of Science and Technology, Yulin 64002, Taiwan.
Po-Yuan WuDepartment of Dermatology, China Medical University Hospital, Taichung 40402, Taiwan.
Yin ChuDepartment of Cosmeceutics, China Medical University, Taichung 40402, Taiwan.
Qiao-Xin ChangDepartment of Cosmeceutics, China Medical University, Taichung 40402, Taiwan.
Kuo-Ching WenDepartment of Cosmeceutics, China Medical University, Taichung 40402, Taiwan.
Chien-Yih LinDepartment of Cosmeceutics, China Medical University, Taichung 40402, Taiwan.
Hsiu-Mei ChiangDepartment of Cosmeceutics, China Medical University, Taichung 40402, Taiwan.ORCID 0000-0002-1586-910X
China Medical University · TWAsia University · TW

Funding

China Medical University CHM106-5-2China Medical University CMU107-BC-7the Ministry of Science and Technology MOST 106-2320-B-039-057-MY3
6 · The paper itself

Abstract

Ultraviolet A (UVA) is a major factor in skin aging and damage. Antioxidative materials may ameliorate this UV damage. This study investigated the protective properties of N-(4-bromophenethyl) caffeamide (K36H) against UVA-induced skin inflammation, apoptosis and genotoxicity in keratinocytes. The protein expression or biofactor concentration related to UVA-induced skin damage were identified using an enzyme-linked immunosorbent assay and western blotting. K36H reduced UVA-induced intracellular reactive oxygen species generation and increased nuclear factor erythroid 2-related factor 2 translocation into the nucleus to upregulate the expression of heme oxygenase-1, an intrinsic antioxidant enzyme. K36H inhibited UVA-induced activation of extracellular-signal-regulated kinases and c-Jun N-terminal kinases, reduced the overexpression of matrix metalloproteinase (MMP)-1 and MMP-2 and elevated the expression of the metalloproteinase-1 tissue inhibitor. Moreover, K36H inhibited the phosphorylation of c-Jun and downregulated

Indexed as

apoptosisDNA damageinflammationN-(4-bromophenethyl) caffeamideoxidative stress

Identifiers

PMID32326032
PMCPMC7222364
OpenAlexW3017124908

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.