Journal of ethnopharmacology · 2026
Compound Dancao Granules inhibits lipid accumulation and hepatocyte apoptosis via the p53 signaling pathway in metabolic dysfunction-associated steatohepatitis mice.
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Li Xutao, Ruan Tianyin, Wang Siyuan, Li Mingyue, Shen Li, Peng Yuan, Zhao Zhimin, Lei Yang, Tao Yanyan
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Metabolic dysfunction-associated steatohepatitis (MASH) is a growing global health burden characterized by hepatic steatosis, inflammation, and fibrosis. Compound Dancao Granules (CDG), a traditional Chinese herbal formula, has shown hepatoprotective potential, yet its underlying molecular mechanisms in treating MASH remain to be elucidated.
AIM OF THE STUDY: This study aimed to investigate the therapeutic efficacy of CDG against MASH and to decipher the molecular mechanisms.
MATERIALS AND METHODS: Two MASH mouse models were established: the first model was established by feeding a high-fat diet (HFD) and subcutaneous injection of CCl4 for 6 weeks; the second model was established by feeding a methionine and choline deficient (MCD) diet for 8 weeks, followed by CDG treatment, with OCA serving as a positive control. In vitro models were established using free fatty acid (FFA)-induced HepG2 cells and LX-2 cells. First, the chemical components of CDG were identified via UHPLC-Q-Exactive Orbitrap HRMS. Subsequently, transcriptomic analysis was performed to identify potential therapeutic targets. Finally, p53 overexpression plasmids were used to assess whether p53 activation could reverse the protective effects of CDG.
RESULTS: CDG administration significantly ameliorated hepatic steatosis, inflammatory and fibrosis in MASH mice. Transcriptomic profiling revealed that the p53 signaling pathway was markedly suppressed by CDG treatment. In vitro, CDG inhibited lipid accumulation and hepatocyte apoptosis in FFA-induced HepG2 cells. Mechanistically, the activation of p53 signaling partially abrogated the protective effects of CDG against FFA-induced apoptosis. Furthermore, CDG treatment significantly inhibited the migration of LX-2 cells, suggesting its potential in preventing hepatic fibrosis progression.
CONCLUSION: CDG effectively alleviates MASH progression by inhibiting lipid accumulation, inflammation, and fibrosis. These protective effects are associated with the suppression of the p53 signaling pathway, suggesting a potential role of this pathway in the mechanism of action. Our findings provide a scientific basis for the clinical application of CDG in the treatment of MASH.
AIM OF THE STUDY: This study aimed to investigate the therapeutic efficacy of CDG against MASH and to decipher the molecular mechanisms.
MATERIALS AND METHODS: Two MASH mouse models were established: the first model was established by feeding a high-fat diet (HFD) and subcutaneous injection of CCl4 for 6 weeks; the second model was established by feeding a methionine and choline deficient (MCD) diet for 8 weeks, followed by CDG treatment, with OCA serving as a positive control. In vitro models were established using free fatty acid (FFA)-induced HepG2 cells and LX-2 cells. First, the chemical components of CDG were identified via UHPLC-Q-Exactive Orbitrap HRMS. Subsequently, transcriptomic analysis was performed to identify potential therapeutic targets. Finally, p53 overexpression plasmids were used to assess whether p53 activation could reverse the protective effects of CDG.
RESULTS: CDG administration significantly ameliorated hepatic steatosis, inflammatory and fibrosis in MASH mice. Transcriptomic profiling revealed that the p53 signaling pathway was markedly suppressed by CDG treatment. In vitro, CDG inhibited lipid accumulation and hepatocyte apoptosis in FFA-induced HepG2 cells. Mechanistically, the activation of p53 signaling partially abrogated the protective effects of CDG against FFA-induced apoptosis. Furthermore, CDG treatment significantly inhibited the migration of LX-2 cells, suggesting its potential in preventing hepatic fibrosis progression.
CONCLUSION: CDG effectively alleviates MASH progression by inhibiting lipid accumulation, inflammation, and fibrosis. These protective effects are associated with the suppression of the p53 signaling pathway, suggesting a potential role of this pathway in the mechanism of action. Our findings provide a scientific basis for the clinical application of CDG in the treatment of MASH.