ArticleFrontiers in cell and developmental biology2026
Liuwei dihuang decoction attenuates intervertebral disc degeneration by inhibiting TRPA1-Mediated ferroptosis in endplate chondrocytes.
Article in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Liuwei Dihuang Decoction (LWDHD) is a well-known traditional Chinese medicine formula, which occupies an important position in clinical TCM practice. This study aimed to elucidate the therapeutic mechanism of LWDHD against Intervertebral Disc Degeneration(IVDD), with a specific focus on its role in preventing endplate chondrocyte degeneration and its interaction with the TRPA1-ferroptosis axis. Methods: The components of LWDHD were first characterized using high-performance liquid chromatography (HPLC). A mouse model of lumbar spinal instability (LSI) was then established to evaluate the therapeutic effects of LWDHD on IVDD-related pain, behavioral function, and intervertebral disc structure. Furthermore, an IL-1β-induced chondrocyte inflammation model was utilized to assess the impact of LWDHD on chondrocyte proliferation, lipid accumulation, oxidative stress, and ferroptosis. Based on predictions from network pharmacology and molecular docking regarding the key mechanisms of LWDHD against IVDD, core signaling pathways were experimentally validated using specific pharmacological agonists. Results: HPLC-MS analysis identified five representative compounds in LWDHD under both positive and negative ion modes. In a mouse model of LSI, LWDHD administration significantly alleviated discogenic pain and restored motor function. Micro-CT results demonstrated that LWDHD treatment preserved intervertebral disc height, protected the endplate against fibrotic structural degeneration, and reduced ROS accumulation, thereby attenuating ferroptosis-related tissue injury. Correspondingly, in IL-1β-induced chondrocytes, LWDHD suppressed intracellular lipid accumulation and oxidative stress, while also restoring chondrocyte proliferative capacity and upregulating the expression of the ferroptosis-related protein GPX4. Through network pharmacology and molecular docking, TRPA1 was identified as a potential therapeutic target of LWDHD. This finding was further validated by fluorescence co-localization and pharmacological activation, which confirmed the regulatory role of TRPA1 on GPX4. Importantly, the protective effects of LWDHD were abolished upon TRPA1 activation, underscoring its essential role in the observed therapeutic outcomes. Discussion: Our study demonstrates that LWDHD mitigates intervertebral disc degeneration by inhibiting TRPA1, thereby restoring redox homeostasis, preserving ECM integrity, and alleviating pain. This work validates the TRPA1-ferroptosis axis as a key pathogenic driver of IVDD and establishes a mechanistic basis for the evidence-based use and modernization of LWDHD in the treatment of degenerative musculoskeletal diseases.
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