» Articles » PMID: 38680355

Liangxue-Qushi-Zhiyang Decoction Ameliorates DNCB-Induced Atopic Dermatitis in Mice Through the MAPK Signaling Pathway Based on Network Pharmacology

Overview
Journal ACS Omega
Specialty Chemistry
Date 2024 Apr 29
PMID 38680355
Authors
Affiliations
Soon will be listed here.
Abstract

The traditional prescription of Liangxue-Qushi-Zhiyang decoction (LQZ) has been demonstrated to be efficacious in treating atopic dermatitis (AD), a chronic inflammatory skin disorder marked by intense itching, redness, rashes, and skin thickening. Nevertheless, there has been an inadequate systematic exploration of the potential targets, biological processes, and pathways for AD treatment through LQZ. The study objective was to evaluate the efficacy and possible mechanism of LQZ in AD mice. In our study, we identified the primary compounds of LQZ, analyzed hub targets, and constructed a network. Subsequently, the predicted mechanisms of LQZ in AD were experimentally studied and validated in vivo, as determined by network pharmacological analysis. A total of 80 serum components of LQZ were identified through ultra-performance liquid chromatography-electrospray ionization-tandem mass spectrometry (UPLC-ESI-MS/MS), among which 49 compounds were absorbed into the bloodstream. Our results indicated that LQZ targets six putative key factors in the MAPK signaling pathway, which play essential roles in AD, namely, EGFR, p-MAPK1/3, p-MAPK14, IL-1β, IL-6, and TNF-α. We observed spleen coefficient, dermatitis scores, and ear thickness were all downregulated in 2,4-dinitrochlorobenzene (DNCB)-induced mice after LQZ treatment. Histological analysis of the dorsal and ear skin further revealed that LQZ significantly decreased skin inflammation, epidermal thickness, and mast cell numbers compared to the DNCB group. Our study demonstrated the effectiveness of LQZ in reducing epidermal and dermal damage in a mouse model of AD. Furthermore, our findings suggest that downregulating the MAPK signaling pathway could be a potential therapeutic strategy for the treatment of AD.

References
1.
Liu J, Tao Y, Zou X, Liu Q, Meng X, Zhang Y . In vitro and in vivo exploration of the anti-atopic dermatitis mechanism of action of Tibetan medicine Qi-Sai-Er-Sang-Dang-Song decoction. J Ethnopharmacol. 2023; 306:116155. DOI: 10.1016/j.jep.2023.116155. View

2.
Liang X, Huang Y, Pan X, Hao Y, Chen X, Jiang H . Erucic acid from suppresses influenza A virus replication and inflammation and through modulation of NF-κB and p38 MAPK pathway. J Pharm Anal. 2020; 10(2):130-146. PMC: 7192973. DOI: 10.1016/j.jpha.2019.09.005. View

3.
Huang D, Sherman B, Lempicki R . Systematic and integrative analysis of large gene lists using DAVID bioinformatics resources. Nat Protoc. 2009; 4(1):44-57. DOI: 10.1038/nprot.2008.211. View

4.
Tan Y, Huang Z, Liu Y, Li X, Stalin A, Fan X . Integrated serum pharmacochemistry, 16S rRNA sequencing and metabolomics to reveal the material basis and mechanism of Yinzhihuang granule against non-alcoholic fatty liver disease. J Ethnopharmacol. 2023; 310:116418. DOI: 10.1016/j.jep.2023.116418. View

5.
Traidl S, Roesner L, Zeitvogel J, Werfel T . Eczema herpeticum in atopic dermatitis. Allergy. 2021; 76(10):3017-3027. DOI: 10.1111/all.14853. View