ArticleJournal of inflammation research2026
Guilu Erxian Glue Restores Immune Homeostasis in Aplastic Anemia Mice by Regulating Treg Lineage Stability via the miRNA-17/10a and FasL/Fas Signaling Pathways.
Article in Journal of inflammation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: This study investigates the functional role and mechanisms of Guilu Erxian Glue (GEG) in regulating immune homeostasis to treat bone marrow (BM) failure in aplastic anemia (AA). Methods: Differentially expressed miRNAs of AA patients were identified through bioinformatics analysis of the Gene Expression Omnibus (GEO) database, followed by enrichment analysis of the identified miRNAs and their predicted target genes. The chemical profile of GEG was characterized by UPLC-MS/MS. An AA mouse model was established via Results: Bioinformatic analysis of the GSE82095 dataset identified significantly dysregulated miRNAs in T cells from AA patients, specifically miRNA-17-5p and miRNA-10a-5p. Preliminary enrichment analysis indicated that these miRNAs are primarily involved in hypoxic stress, T-cell differentiation, and apoptosis. Subsequently, the downstream target genes of these miRNAs were predicted, and further functional enrichment analysis corroborated that these target genes are critically associated with T-cell differentiation. HPLC-MS/MS identified 22 compounds from the aqueous extract of GEG. In vivo, GEG treatment significantly improved BM histopathology and restored peripheral blood counts. It also reduced the percentages of Tfh, Th1, Th17, and effector memory T cells (Tem) ( Conclusion: Our findings suggest that GEG contributes to Treg lineage stability and survival through the potential modulation of the miRNA-17/IKZF4, miRNA-10a/BCL6, and Fas/FasL signaling axes. These synergistic effects appear to support the remodeling of T-cell homeostasis and restoration of cytokine balance, offering a promising, miRNA-targeted strategy for enhancing AA therapy that warrants further clinical investigation.
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