Evidence map›Paper›PMID 39465158›Full record

ArticlePeerJ2024

Indigo alleviates psoriasis through the AhR/NF-κB signaling pathway: an

Yu Lin, Lihong Yang, Dongxiang Wang, Haiqing Lei, Yuelin Zhang, Wen Sun, Jing Liu

Abstract read
In one paragraph

Article in PeerJ, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Activity ofFrontiers in pharmacology · 2026
    Article
  4. 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.

Yu Lin *Department of Dermatology, the First Clinical Medical School of Guangzhou University of Chinese Medicine, Guangzhou, China.
Lihong Yang *Department of Dermatology, the First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.
Dongxiang WangDepartment of Dermatology, the First Clinical Medical School of Guangzhou University of Chinese Medicine, Guangzhou, China.
Haiqing LeiDepartment of Dermatology, the First Clinical Medical School of Guangzhou University of Chinese Medicine, Guangzhou, China.
Yuelin ZhangDepartment of Dermatology, the First Clinical Medical School of Guangzhou University of Chinese Medicine, Guangzhou, China.
Wen SunDepartment of Dermatology, Jingmen Central Hospital, Jingmen, China.
Jing LiuDepartment of Dermatology, the First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Psoriasis is a chronic inflammatory skin disease. A strong association between the AhR/ NFκB axis and the inflammatory response in psoriasis. Indigo (IDG) has demonstrated significant anti-inflammatory properties. This study aimed to assess the anti-psoriatic efficacy of IDG while investigating the underlying mechanisms involved. Methods: In the Results: LPS stimulation significantly elevated TNF-α, IL-6, and NF-κB mRNA levels, which were notably reduced by IDG treatment. Additionally, IDG significantly enhanced the expression of AhR and CYP1A1 mRNA. Further investigation revealed that IDG facilitated AhR translocation from the cytoplasm to the nucleus. In the IMQ-induced psoriasis-like mouse model, IDG NE substantially ameliorated the severity of skin lesions. Moreover, IDG NE treatment reduced the upregulation of inflammatory cytokines such as IL-6, IL-17A, MCP-1, and TNF-α in IMQ-induced skin lesions. It was also observed that IDG NE treatment increased CYP1A1 protein expression while inhibiting p65 and p-p65 protein expression. Conclusion: IDG emerges as a promising treatment for psoriasis, demonstrating effective therapeutic outcomes. Its mechanism of action is likely linked to the modulation of the AhR/NFκB signaling pathway.

Indexed as

Cytochrome P-450 CYP1A1Disease Models, AnimalNF-kappa BPsoriasisReceptors, Aryl HydrocarbonSignal TransductionAnimalsAnti-Inflammatory AgentsBasic Helix-Loop-Helix ProteinsCytokinesHumansImiquimodMaleMiceMice, Inbred BALB CAHR protein, humanAhr protein, mouseAnti-Inflammatory AgentsBasic Helix-Loop-Helix ProteinsCytochrome P-450 CYP1A1CytokinesImiquimodNF-kappa BReceptors, Aryl HydrocarbonAhRIndigoNF-κBPsoriasis

Identifiers

PMID39465158
PMCPMC11505883

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.