Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Immunoregulatory mechanisms underlying vitexin-mediated attenuation of concanavalin A-induced liver injury.
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Shi Qingmiao, He Yuting, Xing Huiwu, Fu Leiya, Lou Na, Lv Chi, Yang Shuwen, Xue Chen, Shen Shen, Lu Juan, Gu Xinyu
Аннотация
BACKGROUND: Autoimmune hepatitis (AIH) is a chronic inflammatory liver disorder driven by dysregulated lymphocyte activation, yet current immunosuppressive therapies are often limited by severe side effects. Vitexin, a natural flavonoid, exhibits potent immunomodulatory properties, but its specific regulatory mechanisms and therapeutic potential in the AIH remain largely unclear.
METHODS: Using a well-validated concanavalin A (ConA)-induced murine model of AIH, this study implemented a synergistic single-cell strategy, integrating high-dimensional mass cytometry (CyTOF) with single-cell RNA sequencing (scRNA-seq), to systematically explore vitexin-mediated changes of hepatic immune landscape.
RESULTS: Vitexin treatment alleviated ConA-induced hepatic inflammatory injury in a potential dose-dependent manner. CyTOF profiling reveals the vitexin's immunomodulatory function, especially in reprogramming of T cells responses. scRNA-seq further identified transcriptional heterogeneity and intricate intercellular communication networks within T cells. Mechanistically, vitexin treatment is associated with suppressed IFN signaling response and reduced expression of IFN-stimulated genes in Runx2+CD4+ Teff and Cxcr6+CD4+ Trm. Furthermore, transcriptomic data are consistent with the possibility that vitexin shifts Gzmc+CD8+ Teff and Klra1+CD8+ Teff toward pro-apoptotic and exhausted-like transcriptional states.
CONCLUSION: This study demonstrates that vitexin alleviates ConA-induced liver injury by mediating the functional reprogramming of T cells. These findings provide mechanistic insights that may guide future therapeutic development for AIH.
METHODS: Using a well-validated concanavalin A (ConA)-induced murine model of AIH, this study implemented a synergistic single-cell strategy, integrating high-dimensional mass cytometry (CyTOF) with single-cell RNA sequencing (scRNA-seq), to systematically explore vitexin-mediated changes of hepatic immune landscape.
RESULTS: Vitexin treatment alleviated ConA-induced hepatic inflammatory injury in a potential dose-dependent manner. CyTOF profiling reveals the vitexin's immunomodulatory function, especially in reprogramming of T cells responses. scRNA-seq further identified transcriptional heterogeneity and intricate intercellular communication networks within T cells. Mechanistically, vitexin treatment is associated with suppressed IFN signaling response and reduced expression of IFN-stimulated genes in Runx2+CD4+ Teff and Cxcr6+CD4+ Trm. Furthermore, transcriptomic data are consistent with the possibility that vitexin shifts Gzmc+CD8+ Teff and Klra1+CD8+ Teff toward pro-apoptotic and exhausted-like transcriptional states.
CONCLUSION: This study demonstrates that vitexin alleviates ConA-induced liver injury by mediating the functional reprogramming of T cells. These findings provide mechanistic insights that may guide future therapeutic development for AIH.