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Duhuo Jisheng Decoction Mitigates Intervertebral Disc Degeneration via Metabolic Reprogramming and TGF-β/Smad-Driven
Chao Song1,2, Xiaofei Wu1, Chaoqi Chen1
1Department of Orthopedics, The Second Affiliated Hospital of Guangxi University of Chinese Medicine, Nanning City, Guangxi Zhuang Autonomous Region, China.
Biomedical Chromatography : BMC
|July 1, 2026
Summary
Duhuo Jisheng Decoction (DHJSD) treats intervertebral disc degeneration (IVDD) by reprogramming metabolism, regulating the TGF-β pathway, and remodeling autophagy and mitochondria. This multi-omics study reveals DHJSD
Area of Science:
- Integrative Medicine and Pharmacology
- Molecular Biology and Biochemistry
- Systems Biology
Background:
- Intervertebral disc degeneration (IVDD) is a complex condition with unclear therapeutic mechanisms.
- Traditional Chinese Medicine, like Duhuo Jisheng Decoction (DHJSD), shows potential for IVDD treatment.
- The precise molecular pathways, including autophagy and fibrosis, targeted by DHJSD remain largely unelucidated.
Purpose of the Study:
- To systematically investigate the molecular mechanisms of Duhuo Jisheng Decoction (DHJSD) in treating intervertebral disc degeneration (IVDD).
- To explore DHJSD's effects on autophagy, fibrosis, and metabolic pathways.
- To validate findings using a multi-omics approach and functional studies.
Main Methods:
- Network pharmacology identified 254 potential active constituents and regulatory pathways of DHJSD.
- Metabolomics and UHPLC-Q-TOF/MS analyzed metabolic profiles and lipid homeostasis.
- In vitro and in vivo functional studies assessed effects on extracellular matrix, TGF-β signaling, autophagy markers, and animal models of IVDD.
Main Results:
- DHJSD attenuated extracellular matrix and fibrosis markers, reduced BMP2 expression, and decreased TGF-β/Smad2/3 phosphorylation.
- Metabolomic analysis revealed DHJSD reshapes lipid homeostasis via glycerophospholipid and sphingolipid metabolism, impacting TGF-β signaling.
- DHJSD modulated autophagy markers (LC3-II/LC3-I, BCL2, P62) and influenced glycolysis and oxidative phosphorylation, potentially via mitochondrial membrane changes.
Conclusions:
- DHJSD treats IVDD through a network involving metabolic reprogramming, TGF-β pathway regulation, and autophagy/mitochondrial remodeling.
- The findings highlight a multi-target therapeutic strategy for IVDD.
- This study demonstrates the value of integrating multi-omics approaches for understanding traditional medicine's mechanisms.
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