Evidence map›Paper›PMID 26256790›Full record

ArticlePhotochemistry and photobiology2015

Baicalin Protects Keratinocytes from Toll-like Receptor-4 Mediated DNA Damage and Inflammation Following Ultraviolet Irradiation.

Wei Min, Israr Ahmad, Michelle E Chang, Erin M Burns, Qihong Qian, Nabiha Yusuf

Open access · greenAbstract read
In one paragraph

Article in Photochemistry and photobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

15 citing papers in PubMed, 30 citations in OpenAlex.

  1. Baicalein prevents skin damage, tumorigenesis and tumor growth in chronic ultraviolet B-irradiated hairless mice.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2025
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. 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

6 authors at 2 institutions in 2 countries.

Wei MinDepartment of Dermatology and Skin Diseases Research Center, University of Alabama at Birmingham, Birmingham, AL.
Israr AhmadDepartment of Dermatology and Skin Diseases Research Center, University of Alabama at Birmingham, Birmingham, AL.
Michelle E ChangDepartment of Dermatology and Skin Diseases Research Center, University of Alabama at Birmingham, Birmingham, AL.
Erin M BurnsDepartment of Dermatology and Skin Diseases Research Center, University of Alabama at Birmingham, Birmingham, AL.
Qihong QianDepartment of Dermatology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Nabiha YusufDepartment of Dermatology and Skin Diseases Research Center, University of Alabama at Birmingham, Birmingham, AL.
University of Alabama at Birmingham · USSoochow University · CN

Funding

Cancer Prevention & Control Training ProgramR25CA047888 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DEMARK-WAHNEFRIED, WENDY, MENESES, KAREN M · 1988 to 2016
$11.2M
UAB Skin Diseases Research CenterP30AR050948 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ELMETS, CRAIG A · 2004 to 2013
$5.5M
NCI NIH HHS R25 CA047888NCI NIH HHS R25CA47888NIAMS NIH HHS P30 AR050948NIAMS NIH HHS P30AR050948
6 · The paper itself

Abstract

UVB radiation contributes to both direct and indirect damage to the skin including the generation of free radicals and reactive oxygen species (ROS), inflammatory responses, immunosuppression and gene mutations, which can ultimately lead to photocarcinogenesis. A plant-derived flavonoid, baicalin, has been shown to have antioxidant, anti-inflammatory and free radical scavenging activities. Previous studies from our laboratory have shown that in murine skin, Toll-like receptor-4 (TLR4) enhanced both UVB-induced DNA damage and inflammation. The aim of this study was to investigate the efficacy of baicalin against TLR4-mediated processes in the murine keratinocyte PAM 212 cell line. Our results demonstrate that treating keratinocytes with baicalin both before and after UV radiation (100 mJ cm(-2) ) significantly inhibited the level of intracellular ROS and decreased cyclobutane pyrimidine dimers and 8-Oxo-2'-deoxyguanosine (8-oxo-dG)-markers of DNA damage. Furthermore, cells treated with baicalin demonstrated an inhibition of TLR4 and its downstream signaling molecules, MyD88, TRIF, TRAF6 and IRAK4. TLR4 pathway inhibition resulted in NF-κB inactivation and down-regulation of iNOS and COX-2 protein expression. Taken together, baicalin treatment effectively protected keratinocytes from UVB-induced inflammatory damage through TLR pathway modulation.

Indexed as

Toll-Like Receptor 4Ultraviolet RaysAnti-Inflammatory Agents, Non-SteroidalCells, CulturedDNA DamageFlavonoidsHumansKeratinocytesReactive Oxygen SpeciesAnti-Inflammatory Agents, Non-SteroidalbaicalinFlavonoidsReactive Oxygen SpeciesTLR4 protein, humanToll-Like Receptor 4

Identifiers

PMID26256790
PMCPMC4631648
OpenAlexW1842926262

What OpenQuestion holds

Textmetadata
LicenceTDM
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.