Evidence map›Paper›PMID 36267759›Full record

ArticleAnnals of translational medicine2022

Inhibitory effects of isoliquiritin on an atopic dermatitis model through the CD177/JAK2/STAT pathway

Qing Wu, Xiumei Mo, Ying Lin, Junfeng Liu, Siqi Ye, Yu Zhang, Xingxing Fan, Dacan Chen, Fenggen Yan

Open access · diamondAbstract read
In one paragraph

Article in Annals of translational medicine, 2022. 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
1.8field-weighted citation impact, top 17% 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, 10 citations in OpenAlex.

  1. Review
  2. Polynucleotides Enhance Skin Barrier Function and Reduce Inflammation in a 2,4-Dinitrochlorobenzene-Induced Mouse Model of Atopic Dermatitis.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2025
    Article
  3. Article
  4. Article
  5. Review
  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

9 authors at 1 institution in 1 country.

Qing WuThe Second Clinical College of Guangzhou University of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, China.
Xiumei MoDepartment of Dermatology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou, China.
Ying LinDepartment of Dermatology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou, China.
Junfeng LiuDepartment of Dermatology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou, China.
Siqi YeDepartment of Dermatology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou, China.
Yu ZhangDepartment of Dermatology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou, China.
Xingxing FanGuangdong-Hong Kong-Macau Joint Lab on Chinese Medicine and Immune Disease Research, Guangzhou, China.
Dacan ChenDepartment of Dermatology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou, China.
Fenggen YanDepartment of Dermatology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou, China.
Guangzhou University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Atopic dermatitis (AD) is a complex inflammatory skin condition characterized by the proliferation and activation of immune cells in skin. Isoliquiritin (ISO) is an active component purified from Methods: This study investigated the potential effects and possible underlying mechanisms of ISO against AD Results: ISO dose-dependently suppressed the viability of HMC1.1 cells. ISO inhibited the secretion of the proinflammatory factors IL-6 and IL-8 and induced the apoptosis of HMC1.1 cells. ISO suppressed the phosphorylation of CD177, JAK2, STAT1, STAT3, and STAT5, and upregulated the protein expression of BAX and cleaved caspase-3 Conclusions: Collectively, our findings showed that ISO administration decreased skin lesion formation by inhibiting inflammation and enhancing immunomodulation through the CD177/JAK2/STAT signaling pathway.

Indexed as

anti-inflammatory activityAtopic dermatitis (AD)human mast cellisoliquiritin (ISO)Nc/Nga mice

Identifiers

PMID36267759
PMCPMC9577790
OpenAlexW4296988791

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.