Abstract
T cells, especially CD4+ T helper (Th) cells, play a vital role in the pathogenesis of specific autoimmune diseases. Naringenin, a citrus flavonoid, exhibits anti-inflammatory, anti-oxidant, and antitumor properties, which have been verified in animal autoimmune disease models. However, naringenin’s possible effects and molecular mechanisms in T cell-mediated autoimmune diseases are unclear. This review summarizes the findings of previous studies and predicts the target of naringenin in T cell-mediated autoimmune disorders such as multiple sclerosis, inflammatory bowel disease, and rheumatoid arthritis through network pharmacology analysis. We performed DAVID enrichment analysis, protein-protein interaction analysis, and molecular docking to predict the positive effect of naringenin on T cell-mediated autoimmune disorders. Sixteen common genes were screened, among which the core genes were PTGS2, ESR1, CAT, CASP3, MAPK1, and AKT1. The possible molecular mechanism relates to HIF-1, estrogen, TNF, and NF-κB signaling pathways. Our findings have significance for future naringenin treatment of T cell-mediated autoimmune diseases.
Author contributions
Zejin Liu and Junpeng Wang conceived the review. Zejin Liu and Xinli Niu generated the manuscript. Junpeng Wang revised the manuscript. All of the authors have read and approved the final manuscript.
Disclosure statement
No potential conflict of interest was reported by the authors.