Journal of ethnopharmacology · 2025
Total flavonoids of Drynaria fortunei ameliorates rheumatoid arthritis by suppressing P. copri-mediated Th17 cell differentiation.
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Liang Huashi, Li Chengxi, Wang Yumeng, Hu Yangye, Zhao Xuejiao, Luo Niancui, Zhang Qinyu, Li Jianping, Guo Jianming
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Rheumatoid arthritis (RA) is a systemic autoimmune disease with undefined etiology. Recent studies have revealed that gut microbiota dysbiosis, particularly the overgrowth of Prevotella copri (P. copri), is associated with the onset and early development of RA. Thus, targeted modulation of P. copri abundance may represent a novel therapeutic strategy for RA. Total flavonoids of Drynaria fortunei (TFDF) have demonstrated anti-arthritic activity, yet the underlying mechanism remains unknown.
AIM OF THE STUDY: This study aimed to elucidate the mechanism by which TFDF ameliorates RA from the perspective of gut microbiota, utilizing collagen-induced arthritis (CIA) mouse model.
MATERIALS AND METHODS: The CIA mouse model was used to investigate the therapeutic effect of TFDF on the RA pathological process. Bacterial colonization experiments were conducted to assess the role of P. copri in Th17 cell differentiation and RA progression, as well as the changes following TFDF treatment.
RESULTS: TFDF significantly alleviated joint inflammation in CIA mice while specifically suppressing intestinal P. copri proliferation. Further bacterial colonization experiments confirmed that P. copri exacerbated RA pathology by promoting Th17 cell differentiation. Whereas, TFDF intervention attenuated arthritis symptoms by inhibiting both P. copri expansion and Th17 cell differentiation.
CONCLUSIONS: These findings indicate that TFDF improves RA by suppressing P. copri-mediated Th17 cell differentiation. This study not only reveals a novel mechanism of TFDF in RA treatment but also provides experimental evidence for microbiota-targeted therapeutic strategies against RA.
AIM OF THE STUDY: This study aimed to elucidate the mechanism by which TFDF ameliorates RA from the perspective of gut microbiota, utilizing collagen-induced arthritis (CIA) mouse model.
MATERIALS AND METHODS: The CIA mouse model was used to investigate the therapeutic effect of TFDF on the RA pathological process. Bacterial colonization experiments were conducted to assess the role of P. copri in Th17 cell differentiation and RA progression, as well as the changes following TFDF treatment.
RESULTS: TFDF significantly alleviated joint inflammation in CIA mice while specifically suppressing intestinal P. copri proliferation. Further bacterial colonization experiments confirmed that P. copri exacerbated RA pathology by promoting Th17 cell differentiation. Whereas, TFDF intervention attenuated arthritis symptoms by inhibiting both P. copri expansion and Th17 cell differentiation.
CONCLUSIONS: These findings indicate that TFDF improves RA by suppressing P. copri-mediated Th17 cell differentiation. This study not only reveals a novel mechanism of TFDF in RA treatment but also provides experimental evidence for microbiota-targeted therapeutic strategies against RA.