Frontiers in pharmacology · 2026
Potential efficacy and preliminary mechanistic insights of the Jianpi Yishen Zhuanggu Tongluo formula for rheumatoid arthritis with sarcopenia-osteopenia: an integrated pilot study.
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Liang Weidong, Chen Liuting, Zhang Yadan, Peng Jianhong
Аннотация
OBJECTIVES: To explore the potential efficacy and identify preliminary metabolic biomarkers of the Jianpi Yishen Zhuanggu Tongluo formula (JPYSZGT) in rheumatoid arthritis (RA) complicated with sarcopenia-osteopenia (SO) using 1H-NMR-based metabolomics and in vitro experiments.
METHODS: In this pilot study, forty RA-SO patients were randomly allocated into a treatment group (Group C, n = 20) receiving JPYSZGT plus conventional therapy and a control group (Group D, n = 20) receiving conventional therapy alone for 12 months. Clinical outcomes, including inflammatory markers (CRP, ESR), bone metabolism markers (CTX, PINP), insulin-like growth factor (IGF), cytokines (IL-6, TNF-α), bone mineral density (BMD), and appendicular skeletal muscle mass index (ASMI), were analyzed.
RESULTS: Compared to Group D, Group C showed greater improvements in DAS28-ESR, ASMI, and BMD, and greater reductions in ESR, CRP, TNF-α, CTX, and PINP, along with a significant increase in IGF levels. Metabolomics analysis identified preliminary alterations in 14 pathways involving glucose, lipid, and amino acid metabolisms. In vitro experiments suggested that JPYSZGT may suppress macrophage activation, potentially upregulate PINK1/PARKIN, downregulate OPG/RANK pathways, and reduce TNF-α and IL-6 secretion.
CONCLUSION: This exploratory study suggests that JPYSZGT may improve bone-muscle metrics in RA-SO and that its potential mechanisms could involve the modulation of the PINK1/PARKIN, OPG/RANK, and PI3K/Akt pathways. It also appears to inhibit macrophage-driven inflammation. These findings warrant further investigation in larger-scale studies.
CLINICAL TRIAL REGISTRATION: identifier ChiCTR2500106729.
METHODS: In this pilot study, forty RA-SO patients were randomly allocated into a treatment group (Group C, n = 20) receiving JPYSZGT plus conventional therapy and a control group (Group D, n = 20) receiving conventional therapy alone for 12 months. Clinical outcomes, including inflammatory markers (CRP, ESR), bone metabolism markers (CTX, PINP), insulin-like growth factor (IGF), cytokines (IL-6, TNF-α), bone mineral density (BMD), and appendicular skeletal muscle mass index (ASMI), were analyzed.
RESULTS: Compared to Group D, Group C showed greater improvements in DAS28-ESR, ASMI, and BMD, and greater reductions in ESR, CRP, TNF-α, CTX, and PINP, along with a significant increase in IGF levels. Metabolomics analysis identified preliminary alterations in 14 pathways involving glucose, lipid, and amino acid metabolisms. In vitro experiments suggested that JPYSZGT may suppress macrophage activation, potentially upregulate PINK1/PARKIN, downregulate OPG/RANK pathways, and reduce TNF-α and IL-6 secretion.
CONCLUSION: This exploratory study suggests that JPYSZGT may improve bone-muscle metrics in RA-SO and that its potential mechanisms could involve the modulation of the PINK1/PARKIN, OPG/RANK, and PI3K/Akt pathways. It also appears to inhibit macrophage-driven inflammation. These findings warrant further investigation in larger-scale studies.
CLINICAL TRIAL REGISTRATION: identifier ChiCTR2500106729.