Molecular biology reports · 2026
Panax notoginseng saponins (PNS)alleviates rheumatoid arthritis by regulating HIF-1α/PKM2-mediated glycolysis to inhibit Th17 differentiation.
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Bao Yujie, Chen Shuoyu, Ge Yu, Zhang Qiaoyu, Wang Furong, Jiang Baoping, Zhou Lingling
Аннотация
PURPOSE: To assess Panax notoginseng saponins(PNS)'s therapeutic potential against RA and its modulation of Th17 differentiation, specifically the in vitro mechanism by which PNS inhibits Th17 cell glycolysis via the HIF-1α pathway.
METHODS: Collagen-induced arthritis (CIA) mouse model was established by immunization with type II collagen. CIA mice were randomly divided into control, model, and PNS (100 mg/kg) treatment groups. Network pharmacology was employed to identify PNS active components and RA-related targets; protein-protein interaction (PPI) network construction and pathway enrichment analysis were used to predict core targets. Naive CD4⁺T cells were induced to differentiate into Th17 cells with interleukin (IL)-6, IL-23, and transforming growth factor-β (TGF-β), and treated with PNS at concentrations of 5, 10, and 20 µg/mL). Th17 differentiation, IL-17 A secretion, and pathway-related molecules were detected by flow cytometry, ELISA, RT-qPCR, and immunoblotting. Compound 3 K and DFOM validated the mechanism.
RESULTS: PNS attenuated CIA severity (reduced hind paw swelling, arthritis scores, improved body weight, alleviated pathology). KEGG linked Th17 differentiation, PKM2, HIF-1α to PNS's anti-RA effects. PNS reduced Th17 ratios, inhibited PKM2/HIF-1α expression, suppressed PKM2-mediated glycolysis, and reversed HIF-1α hyperactivation in Th17 cells.
CONCLUSIONS: PNS relieves CIA by inhibiting Th17 differentiation via suppressing HIF-1α-mediated PKM2 expression and glycolysis-dependent Th17 differentiation.
METHODS: Collagen-induced arthritis (CIA) mouse model was established by immunization with type II collagen. CIA mice were randomly divided into control, model, and PNS (100 mg/kg) treatment groups. Network pharmacology was employed to identify PNS active components and RA-related targets; protein-protein interaction (PPI) network construction and pathway enrichment analysis were used to predict core targets. Naive CD4⁺T cells were induced to differentiate into Th17 cells with interleukin (IL)-6, IL-23, and transforming growth factor-β (TGF-β), and treated with PNS at concentrations of 5, 10, and 20 µg/mL). Th17 differentiation, IL-17 A secretion, and pathway-related molecules were detected by flow cytometry, ELISA, RT-qPCR, and immunoblotting. Compound 3 K and DFOM validated the mechanism.
RESULTS: PNS attenuated CIA severity (reduced hind paw swelling, arthritis scores, improved body weight, alleviated pathology). KEGG linked Th17 differentiation, PKM2, HIF-1α to PNS's anti-RA effects. PNS reduced Th17 ratios, inhibited PKM2/HIF-1α expression, suppressed PKM2-mediated glycolysis, and reversed HIF-1α hyperactivation in Th17 cells.
CONCLUSIONS: PNS relieves CIA by inhibiting Th17 differentiation via suppressing HIF-1α-mediated PKM2 expression and glycolysis-dependent Th17 differentiation.