Evidence map›Paper›PMID 34044769›Full record

ArticleBMC immunology2021

Glycyrrhizin improves the pathogenesis of psoriasis partially through IL-17A and the SIRT1-STAT3 axis.

Huang Qiong, Ling Han, Nanxue Zhang, Huyan Chen, Kexiang Yan, Zhenghua Zhang, Ying Ma, Jinhua Xu

Open access · goldAbstract read
In one paragraph

Article in BMC immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Huang Qiong *Department of Dermatology, Huashan Hospital Affiliated to Fudan University, Shanghai, 200040, China.
Ling Han *Department of Dermatology, Huashan Hospital Affiliated to Fudan University, Shanghai, 200040, China.
Nanxue Zhang *Department of Dermatology, Huashan Hospital Affiliated to Fudan University, Shanghai, 200040, China.
Huyan ChenDepartment of Dermatology, Huashan Hospital Affiliated to Fudan University, Shanghai, 200040, China.
Kexiang YanDepartment of Dermatology, Huashan Hospital Affiliated to Fudan University, Shanghai, 200040, China.
Zhenghua ZhangDepartment of Dermatology, Huashan Hospital Affiliated to Fudan University, Shanghai, 200040, China.
Ying MaDepartment of Dermatology, Huashan Hospital Affiliated to Fudan University, Shanghai, 200040, China. yingmayingma@126.com.
Jinhua XuDepartment of Dermatology, Huashan Hospital Affiliated to Fudan University, Shanghai, 200040, China. jinhuaxu1989@163.com.
Fudan University · CNHuashan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe anti-inflammatory effect of glycyrrhizin has been widely recognized, while the specific mechanism of glycyrrhizin in psoriasis remains poorly understood.

resultsIn the imiquimod-induced mouse model of psoriasis (IMD), we found that glycyrrhizin can substantially improve the adverse symptoms in mice. The hematoxylin-eosin staining results showed that glycyrrhizin can also improve the pathological state of skin cells in IMD mice. Using enzyme-linked immunosorbent assay (ELISA), we found that glycyrrhizin substantially inhibited the expression of IL-17A and IFN-γ in the serum of IMD mice. In order to simulate the effect of IL-17A on keratinocytes in psoriasis, we treated HaCaT cells with 100 ng/mL IL-17A (IL-17A-HaCaT cells) for 48 h. Then, using cell-counting kit-8 (CCK-8) and ELISA assays, we found that glycyrrhizin inhibited the proliferation of IL-17A-HaCaT cells and reversed the promotion of IL-6, CCL20, and TNF-α induced by IL-17A. Further, western blotting (WB) results indicated that glycyrrhizin promoted the expression of SIRT1 and inhibited the expression of STAT3 and phosphorylated STAT3 (p-STAT3). By treating IL-17A-HaCaT cells with EX-527 (a potent and selective inhibitor of SIRT1), combined with CCK-8 and WB experiments, we initially found that EX-527 inhibited the proliferation of IL-17A-HaCaT cells and promoted the expression of STAT3, p-STAT3, and acetylated STAT3 (a-STAT3). However, when glycyrrhizin was added at the same time, the proliferation of IL-17A-HaCaT cells increased, and the expression of STAT3, p-STAT3, and a-STAT3 reduced. We then knocked down the expression of SIRT1 via small interfering RNA in IL-17A-HaCaT cells, and the results were consistent with those of EX-527.

conclusionsTogether, these results indicated that glycyrrhizin improved psoriasis by inhibiting the expression of IL-17A and IFN-γ in vivo and suppressed the proliferation of IL-17A-HaCaT cells and the expression of STAT3, p-STAT3, and a-STAT3 by upregulating SIRT1 in vitro.

Indexed as

AdultAnimalsAnti-Inflammatory AgentsCarbazolesDisease Models, AnimalFemaleGlycyrrhizaGlycyrrhizic AcidHaCaT CellsHumansImiquimodInterleukin-17MicePsoriasisRNA, Small InterferingSirtuin 16-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamideAnti-Inflammatory AgentsCarbazolesGlycyrrhizic AcidImiquimodInterleukin-17RNA, Small InterferingSirtuin 1STAT3 Transcription FactorGlycyrrhizinIL-17APsoriasisSIRT1-STAT3 pathway

Identifiers

PMID34044769
PMCPMC8161965
OpenAlexW3118465751

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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.