Evidence map›Paper›PMID 28114924›Full record

ArticleBMC complementary and alternative medicine2017

N-(4-methoxyphenyl) caffeamide-induced melanogenesis inhibition mechanisms.

Yueh-Hsiung Kuo, Chien-Chia Chen, Po-Yuan Wu, Chin-Sheng Wu, Ping-Jyun Sung, Chien-Yih Lin, Hsiu-Mei Chiang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC complementary and alternative medicine, 2017. 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
1.0field-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, 12 citations in OpenAlex.

  1. Article
  2. Tuliposides H-J and Bioactive Components from the Bulb ofMolecules (Basel, Switzerland) · 2021
    Article
  3. Antimelanogenesis Effects of Theasinensin A.International journal of molecular sciences · 2021
    Article
  4. Article
  5. Article
  6. 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

7 authors at 4 institutions in 1 country.

Yueh-Hsiung KuoDepartment of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, China Medical University, Taichung, 404, Taiwan.
Chien-Chia ChenDepartment of Cosmeceutics, China Medical University, Taichung, 404, Taiwan.
Po-Yuan WuDepartment of Dermatology, China Medical University Hospital, Taichung, 404, Taiwan.
Chin-Sheng WuDepartment of Cosmeceutics, China Medical University, Taichung, 404, Taiwan.
Ping-Jyun SungNational Museum of Marine Biology and Aquarium, Pingtung, 944, Taiwan.
Chien-Yih LinDepartment of Biotechnology, Asia University, Taichung, 413, Taiwan.
Hsiu-Mei ChiangDepartment of Cosmeceutics, China Medical University, Taichung, 404, Taiwan. hmchiang@mail.cmu.edu.tw.
China Medical University · TWAsia University · TWChina Medical University Hospital · TWNational Museum of Marine Biology and Aquarium · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe derivative of caffeamide exhibits antioxidant and antityrosinase activity. The activity and mechanism of N-(4-methoxyphenyl) caffeamide (K36E) on melanogenesis was investigated.

methodsB16F0 cells were treated with various concentrations of K36E; the melanin contents and related signal transduction were studied. Western blotting assay was applied to determine the protein expression, and spectrophotometry was performed to identify the tyrosinase activity and melanin content.

resultsOur results indicated that K36E reduced α-melanocyte-stimulating hormone (α-MSH)-induced melanin content and tyrosinase activity in B16F0 cells. In addition, K36E inhibited the expression of phospho-cyclic adenosine monophosphate (cAMP)-response element-binding protein, microphthalmia-associated transcription factor (MITF), tyrosinase, and tyrosinase-related protein-1 (TRP-1). K36E activated the phosphorylation of protein kinase B (AKT) and glycogen synthase kinase 3 beta (GSK3β), leading to the inhibition of MITF transcription activity. K36E attenuated α-MSH induced cAMP pathways, contributing to hypopigmentation.

conclusionsK36E regulated melanin synthesis through reducing the expression of downstream proteins including p-CREB, p-AKT, p-GSK3β, tyrosinase, and TRP-1, and activated the transcription factor, MITF. K36E may have the potential to be developed as a skin whitening agent.

Indexed as

AnilidesAnimalsCaffeic AcidsCell Line, TumorCyclic AMP Response Element-Binding ProteinGlycogen Synthase Kinase 3 betaInterferon Type IMelaninsMiceMicrophthalmia-Associated Transcription FactorMonophenol MonooxygenasePregnancy ProteinsProto-Oncogene Proteins c-aktSignal TransductionSkin Lightening PreparationsAnilidesCaffeic AcidsCyclic AMP Response Element-Binding ProteinGlycogen Synthase Kinase 3 betainterferon tauInterferon Type IMelaninsMicrophthalmia-Associated Transcription FactorMitf protein, mouseMonophenol MonooxygenaseN-(4-methoxyphenyl)caffeamidePregnancy ProteinsProto-Oncogene Proteins c-aktSkin Lightening PreparationscAMP response element-binding proteinGlycogen synthase kinase 3 betaMelanogenesisMicrophthalmia-associated transcription factorN-(4-methoxyphenyl) caffeamidePropolis

Identifiers

PMID28114924
PMCPMC5259883
OpenAlexW2581362881

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.