Evidence map›Paper›PMID 37602424›Full record

ArticlePharmaceutical biology2023

Icariin restrains NLRP3 inflammasome-mediated Th2 immune responses and ameliorates atopic dermatitis through modulating a novel lncRNA MALAT1/miR-124-3p axis.

Wei Zhao, Huan-Huan Yu, Wei-Wei Meng, Ai-Min Liu, Bu-Xin Zhang, Ying Wang, Jie Li, Li Wang, Yu-Fu Fang

Open access · goldAbstract read
In one paragraph

Article in Pharmaceutical biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

20 citing papers in PubMed, 22 citations in OpenAlex.

  1. Global deletion ofbioRxiv : the preprint server for biology · 2026
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  12. The role of microRNAs in atopic dermatitis.Non-coding RNA research · 2024
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  17. Article
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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.

Wei ZhaoDermatology Department, The Second Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China.
Huan-Huan YuDermatology Department, The Second Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China.
Wei-Wei MengDermatology Department, The Second Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China.
Ai-Min LiuDermatology Department, The Second Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China.
Bu-Xin ZhangDermatology Department, The Second Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China.
Ying WangDermatology Department, The Second Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China.
Jie LiDermatology Department, The Second Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China.
Li WangDermatology Department, The Second Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China.
Yu-Fu FangDermatology Department, The Second Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China.ORCID 0000-0001-9656-5281
Henan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

contextAtopic dermatitis (AD) is a common inflammatory skin disease characterized with hyperactivation of type 2 T helper (Th2) immune responses. Icariin is a flavonoid glucoside with anti-inflammatory activities, which has been used to treat multiple diseases.

objectiveThe present study investigates the underlying mechanisms by which icariin regulates Th2 responses and AD development. MATERIALS AND

methodsBALB/c mice were induced by DNFB to establish AD models, and injected with or without 10 mg/kg icariin for 2 weeks (i.p., daily). CD4

resultsIcariin ameliorated AD-like skin lesion, manifested as a significant decrease in dermatitis scores (from 8.00 ± 1.00 to 3.67 ± 0.58), serum IgE levels (from 3119.15 ± 241.81 to 948.55 ± 182.51 ng/mL), epidermal thickness (from 93.86 ± 4.61 to 42.67 ± 2.48 µm) and infiltration of mast cells (from 60.67 ± 3.21 cells to 36.00 ± 2.65 cells). Also, icariin inactivated NLRP3 inflammasome, inhibited Th2 skewing, reduced lncRNA MALAT1 expression, but elevated miR-124-3p expression DISCUSSION AND

conclusionsThe findings further improve our understanding of the mechanism by which icariin affects AD progression, and highlights the potential of icariin in the treatment of AD.

Indexed as

Dermatitis, AtopicMicroRNAsRNA, Long NoncodingAnimalsFlavonoidsInflammasomesMiceMice, Inbred BALB CNLR Family, Pyrin Domain-Containing 3 ProteinFlavonoidsicariinInflammasomesMicroRNAsMirn124 microRNA, mouseNLR Family, Pyrin Domain-Containing 3 ProteinRNA, Long NoncodingCD4+T cellsMALAT1miR-124-3pNLRP3Th2 responses

Identifiers

PMID37602424
PMCPMC10444017
OpenAlexW4386019542

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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.