Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Huzhang-Xiangbaji compounds enhance the repair of meniscal cartilage by inhibiting ferroptosis and inflammatory microenvironment.
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Li Jiehan, Zhou Jiahui, Zhang Ge, Ding Ning, Kuang Zhengming, Wang Junqiang, Liu Nannan, Jia Guiyun, Jiang Meimei, Wu Siming, Yang Jie, Ding Xuan, Lei Zhiguang, Nie Yiqiong, Zhang Yingjie, Li Qian
Аннотация
BACKGROUND: Meniscus injury (MI) is a common orthopedic condition for which effective therapeutic strategies remain limited. Conventional treatments often yield suboptimal outcomes, whereas traditional Chinese medicine (TCM) has shown promising advantages in managing MI. In this study, we investigated the therapeutic efficacy of the TCM formulation Huzhang-Xiangbaji (HZ-XBJ) compounds in treating MI, as well as the underlying mechanisms involved in meniscal cartilage repair.
METHODS: The therapeutic effects of HZ-XBJ compounds on MI were evaluated using in vivo models. Subsequently, compound-target networks were constructed through Ultra-Performance Liquid Chromatography-Mass Spectrometry combined with network pharmacology. Key therapeutic targets, including PTGS2, were identified by topological analysis and molecular docking, followed by validation with surface plasmon resonance analysis and enzymatic inhibition assays. The molecular mechanism was further explored through a series of in vitro experiments, including PTGS2 overexpression assays, CCK-8 assays, EdU assays, qRT-PCR, Western blot, and flow cytometry, among others.
RESULTS: HZ-XBJ compounds significantly enhanced chondrocyte proliferation and collagen synthesis, thereby facilitating cartilage repair both in vitro and in vivo. Mechanistically, HZ-XBJ compounds inhibited PTGS2 activity, reducing lipid peroxidation and ferroptosis in chondrocytes. In terms of anti-inflammatory regulation, HZ-XBJ compounds decreased PGE2 secretion via PTGS2 inhibition, subsequently attenuating activation of the EP4-cAMP/PKA/ERK signaling pathway in dendritic cells and reducing their maturation.
CONCLUSION: HZ-XBJ compounds exert therapeutic effects on MI by directly inhibiting PTGS2, thereby preventing chondrocyte ferroptosis and suppressing dendritic cell maturation through reduced PGE2 production. These findings highlight HZ-XBJ compounds as a novel therapeutic strategy for MI.
METHODS: The therapeutic effects of HZ-XBJ compounds on MI were evaluated using in vivo models. Subsequently, compound-target networks were constructed through Ultra-Performance Liquid Chromatography-Mass Spectrometry combined with network pharmacology. Key therapeutic targets, including PTGS2, were identified by topological analysis and molecular docking, followed by validation with surface plasmon resonance analysis and enzymatic inhibition assays. The molecular mechanism was further explored through a series of in vitro experiments, including PTGS2 overexpression assays, CCK-8 assays, EdU assays, qRT-PCR, Western blot, and flow cytometry, among others.
RESULTS: HZ-XBJ compounds significantly enhanced chondrocyte proliferation and collagen synthesis, thereby facilitating cartilage repair both in vitro and in vivo. Mechanistically, HZ-XBJ compounds inhibited PTGS2 activity, reducing lipid peroxidation and ferroptosis in chondrocytes. In terms of anti-inflammatory regulation, HZ-XBJ compounds decreased PGE2 secretion via PTGS2 inhibition, subsequently attenuating activation of the EP4-cAMP/PKA/ERK signaling pathway in dendritic cells and reducing their maturation.
CONCLUSION: HZ-XBJ compounds exert therapeutic effects on MI by directly inhibiting PTGS2, thereby preventing chondrocyte ferroptosis and suppressing dendritic cell maturation through reduced PGE2 production. These findings highlight HZ-XBJ compounds as a novel therapeutic strategy for MI.