AI Article Synopsis
- Non-alcoholic fatty liver disease (NAFLD) is a rising global health issue with no approved effective treatments, prompting researchers to explore traditional remedies like the Yindanxinnaotong (YDX) formula from traditional Chinese medicine.
- This study examined the effects of YDX on NAFLD in mice fed a high-fat diet, assessing various health indicators, gut microbiota, and gene expression related to liver function and metabolism.
- Results showed that YDX not only reduced body weight and liver inflammation but also improved lipid profiles, insulin sensitivity, and gut microbial diversity, suggesting its potential as a protective treatment for NAFLD.
Article Abstract
Backgroud: Non-alcoholic fatty liver disease (NAFLD) is a growing chronic liver disease worldwide, and no effective agent is approved yet for this condition. Traditional Chinese Medicine (TCM), which has been practiced for thousands of years in China and other Asian countries, is considered an important source for identifying novel medicines for various diseases. Miao medicine Yindanxinnaotong formula (YDX) is a classical TCM for the treatment of hyperlipidemia disease by reducing blood lipid content, while the role of YDX have not been clarified in NAFLD.
Purpose: To investigate the protective effect of YDX on NAFLD in mice induced by high fat diet (HFD) and clarify the potential mechanism.
Methods: NAFLD mice model was constructed by receiving HFD for 10-week period with or without YDX administration. Lipid profiles, biochemical indicators, and histopathological staining were performed to evaluate the extent of hepatic lipid accumulation and hepatic steatosis. 16S rRNA sequencing was used to determine the gut microbial composition. Serum metabolomics was further used to investigate the changes in plasma biomarkers for NAFLD-associated by UPLC-Q-TOF/MS analysis. Subsequently, liver transcriptomics was employed to identify differentially expressed genes and explore regulatory pathways. Then, lipid metabolism-related proteins and inflammation factors were examined by Western blot and ELISA.
Results: YDX reduced body weight gain, liver index and inflammatory cytokines levels, along with improved hepatic steatosis, serum lipid profile, sensitivity to insulin and also tolerance to glucose, and enhanced oxidative defense system in HFD-induced mice. Also, YDX remarkedly affected gut microbiota diversity and community richness and decreased the ratio of Firmicutes/Bacteroidetes. Meanwhile, YDX also reduced the production of harmful lipid metabolites in the sera of NAFLD mice, such as LPC(18:0), LPC(18:1) and carnitine. Notably, consistent with liver transcriptomics results, YDX downregulated the expression of proteins implicated in de novo lipid synthesis (Srebp-1c, Acaca, Fasn, Scd-1, and Cd36) and pro-inflammatory cytokines (IL-6 and TNF-α), and increased the expression of proteins-related fatty acid β-oxidation (Ampkα, Ppar-α, and Cpt-1) in the liver by activating Ampk pathway.
Conclusion: YDX is promisingly an effective therapy for preventing NAFLD by modulating the Ampk pathway, inhibiting gut microbiota disorder, and reducing the production of harmful lipid metabolites.
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| http://dx.doi.org/10.1016/j.phymed.2024.156026 | DOI Listing |
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