Evidence map›Paper›PMID 38379039›Full record

ArticleBiochemical genetics2024

Daturataturin A Ameliorates Psoriasis by Regulating PPAR Pathway.

Zheng Wei, Hongfa Zhong, Shanmin Yuan, Cong Chen

Abstract read
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In one paragraph

Article in Biochemical genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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.

Zheng WeiDepartment of Traditional Chinese Medicine, Ganzhou People's Hospital, No. 16 Meiguang Avenue, Ganzhou City, 341000, Jiangxi Province, China.
Hongfa ZhongTrauma Center, Ganzhou People's Hospital, No. 16 Meiguang Avenue, Ganzhou City, 341000, Jiangxi Province, China.
Shanmin YuanDepartment of Traditional Chinese Medicine, Ganzhou People's Hospital, No. 16 Meiguang Avenue, Ganzhou City, 341000, Jiangxi Province, China.
Cong ChenDepartment of Traditional Chinese Medicine, Ganzhou People's Hospital, No. 16 Meiguang Avenue, Ganzhou City, 341000, Jiangxi Province, China. cbs1215@sina.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriasis is a kind of severe immune-mediated systemic skin disorder, becoming a worldwide public health concern. Daturataturin A (DTA), a withanolide compound, exerts excellent anti-inflammatory and anti-proliferative properties. The objective of this study is to elucidate the effect of DTA on psoriasis and its potential mechanism. We established psoriasis-like keratinocytes model by stimulating HaCaT cells with M5 cocktail cytokines including Interleukin (IL)-17A, IL-22, oncostatin M, IL-1α, and tumor necrosis factor-α (TNF-α), followed by intervention with DTA. The potential effects and mechanisms of DTA on psoriasis were evaluated in vitro. DTA was found to be able to inhibit hyperproliferation, promote apoptosis, decrease the release of pro-inflammatory cytokines, downregulate keratin expression, and improve lipid metabolism via regulating the peroxisome proliferator-activated receptor (PPAR) signaling pathway by M5 cocktail cytokines stimulation in HaCaT cells. DTA ameliorated lipid metabolism of psoriasis and exerted the potential anti-psoriasis effects by regulating PPAR pathway in vitro, suggesting that DTA may act as a new therapeutic agent for psoriasis.

Indexed as

KeratinocytesPsoriasisSignal TransductionApoptosisCell LineCell ProliferationCytokinesHaCaT CellsHumansLipid MetabolismPeroxisome Proliferator-Activated ReceptorsCytokinesPeroxisome Proliferator-Activated ReceptorsDaturataturin ALipid metabolismPPAR signaling pathwayPsoriasisTherapeutic agent

Identifiers

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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.