ArticleVirus research2025
Regulation of inflammatory cytokines and activation of PI3K/Akt pathway by Yiqi Jiedu Formula in recurrent Herpes Simplex Keratitis: Experimental and network pharmacology evidence.
Article in Virus research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- HDAC11-Mediated Deacetylation of Triosephosphate Isomerase 1 Promotes Idiopathic Pulmonary Fibrosis.Research (Washington, D.C.) · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study investigates the therapeutic effects of the Yiqi Jiedu (YQJD) formula on Herpes Simplex Keratitis (HSK) induced by herpes simplex virus type 1 (HSV-1) and elucidates its mechanisms of action through experimental and network pharmacology approaches.
methodsActive ingredients of the YQJD formula were identified using UPLC-HRMS. Network pharmacology was employed to predict shared targets between YQJD and HSK, focusing on the PI3K/Akt signaling pathway. Molecular docking was performed to assess the interaction between key ingredients and targets. In vivo, an HSK mouse model was used to evaluate the YQJD formula's impact on corneal lesions and inflammatory factors. In vitro, human corneal epithelial cells (HCECs) were infected with HSV-1 to assess the formula's effect on IL-4 expression.
resultsUPLC-HRMS identified 34 compounds in YQJD, with Isovitexin and Formononetin exhibiting high oral bioavailability. Network analysis revealed 97 intersecting targets, implicating the PI3K/Akt pathway in YQJD's mechanism. Molecular docking showed strong affinities between IL-4, IL-6, and YQJD compounds. In vivo, YQJD significantly improved corneal lesions and modulated the expression of IL-4, IL-6, and AKT. In vitro, YQJD-containing serum regulated IL-4 expression in HCECs post-HSV-1 infection.
conclusionThe YQJD formula ameliorates Herpes Simplex Keratitis by regulating inflammatory cytokines and activating the PI3K/Akt pathway, offering a potential therapeutic strategy for HSK.
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