Journal of ethnopharmacology · 2025
The Jieduquyuziyin prescription alleviates systemic lupus erythematosus by modulating B cell metabolic reprogramming via the AMPK/PKM2 signaling pathway.
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Li Xiaolong, Zhu Qingmiao, Yang Zi, Zhu Mengyu, Xie ZhiJun, Fan Yongsheng, Zhao Ting
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: The Jieduquyuziyin prescription (JP) is an enhanced formula derived from the "Sheng Ma Bie Jia Tang" in the Golden Chamber. JP is an empirical formula approved for use in the treatment of systemic lupus erythematosus (SLE) in hospitals across China, demonstrating notable therapeutic effects. It has been shown to suppress B cell activation and alleviate symptoms; however, its underlying mechanism remains unclear.
AIM OF THE STUDY: The aim of this study is to investigate the effect of JP on B cell metabolic reprogramming in the treatment of SLE and to elucidate the underlying regulatory mechanisms.
MATERIALS AND METHODS: Core targets and pathways regulating B cell activation were identified through sequencing of activated and resting B cells from SLE patients and network pharmacology of JP. Targeted metabolomics was employed to assess JP's effect on B cell metabolism. In vivo experiments evaluated the effects of JP, JP combined with a PKM2 inhibitor, or an AMPK inhibitor on SLE activity, B cell activation and glycolysis.
RESULTS: Bioinformatics analyses identified PKM as a core target in B cell activation, which was significantly upregulated and linked to the inhibition of AMPK signaling. JP reduced B cell glycolysis and activation, leading to significant improvements in disease pathology. The combination of JP with an AMPK inhibitor diminished the therapeutic effect. Further studies suggested that JP inhibits glycolysis-dependent B cell activation via the AMPK/PKM2 pathway, reducing germinal center responses and effector B cells.
CONCLUSION: This study reveals that the AMPK/PKM2 pathway is a promising therapeutic target for regulating immune metabolic imbalance in SLE B cells. Additionally, it provides evidence that JP may improve SLE by activating the AMPK/PKM2 pathway to inhibit glycolysis-dependent B cell activation, laying the foundation for further investigation of its therapeutic mechanisms.
AIM OF THE STUDY: The aim of this study is to investigate the effect of JP on B cell metabolic reprogramming in the treatment of SLE and to elucidate the underlying regulatory mechanisms.
MATERIALS AND METHODS: Core targets and pathways regulating B cell activation were identified through sequencing of activated and resting B cells from SLE patients and network pharmacology of JP. Targeted metabolomics was employed to assess JP's effect on B cell metabolism. In vivo experiments evaluated the effects of JP, JP combined with a PKM2 inhibitor, or an AMPK inhibitor on SLE activity, B cell activation and glycolysis.
RESULTS: Bioinformatics analyses identified PKM as a core target in B cell activation, which was significantly upregulated and linked to the inhibition of AMPK signaling. JP reduced B cell glycolysis and activation, leading to significant improvements in disease pathology. The combination of JP with an AMPK inhibitor diminished the therapeutic effect. Further studies suggested that JP inhibits glycolysis-dependent B cell activation via the AMPK/PKM2 pathway, reducing germinal center responses and effector B cells.
CONCLUSION: This study reveals that the AMPK/PKM2 pathway is a promising therapeutic target for regulating immune metabolic imbalance in SLE B cells. Additionally, it provides evidence that JP may improve SLE by activating the AMPK/PKM2 pathway to inhibit glycolysis-dependent B cell activation, laying the foundation for further investigation of its therapeutic mechanisms.