How Sea Buckthorn Compounds Help Improve Fatty Liver Disease: A Study

Jenn Hoskins
11th August, 2024

How Sea Buckthorn Compounds Help Improve Fatty Liver Disease: A Study

Image Source: Natural Science News, 2024

Key Findings

  • Researchers at Qinghai University, China, found that sea buckthorn triterpenoid acid enrichment (STE) can treat non-alcoholic fatty liver disease (NAFLD)
  • STE treatment reduced fat accumulation and improved liver function in mice with NAFLD induced by a high-fat diet
  • The study showed that STE activates the AMPK-SREBP1 pathway, reducing lipid accumulation and inflammation in liver cells
Non-alcoholic fatty liver disease (NAFLD) is a prevalent liver condition linked to metabolic syndrome, characterized by excessive fat accumulation in liver cells. This condition can progress from simple steatosis (benign fat accumulation) to more severe forms like nonalcoholic steatohepatitis (NASH), which involves inflammation, cell death, and fibrosis, potentially leading to cirrhosis and liver cancer[2]. Current treatments are limited, highlighting the need for new therapeutic approaches. A recent study conducted by researchers at Qinghai University, China, explored the potential of sea buckthorn triterpenoid acid enrichment (STE) in treating NAFLD[1]. Sea buckthorn (Hippophae rhamnoides L.) has a long history in traditional Chinese medicine for treating various ailments, but its specific effects on NAFLD were not well understood. This study aimed to elucidate the pharmacological efficacy and underlying mechanisms of STE in NAFLD treatment. The researchers employed a combination of network pharmacology and experimental validation in vitro (cell models) and in vivo (animal models). They first identified potential targets of triterpenoid acid compounds from databases and constructed a protein-protein interaction (PPI) network to pinpoint crucial targets. Enrichment analysis using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways predicted the signaling pathways affected by STE. Key targets such as AKT1, TNF, IL6, INS, JUN, STAT3, and TP53 were identified, with the AMPK-SREBP1 pathway being particularly significant. In the animal experiments, NAFLD was induced in mice through a high-fat diet. STE treatment significantly reduced levels of triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), alanine transaminase (ALT), and aspartate aminotransferase (AST), while increasing high-density lipoprotein cholesterol (HDL-C). These improvements were corroborated by histological analysis, which showed reduced fat accumulation in liver and epididymal fat tissues. In vitro, the researchers used HepG2 cells (a human liver cancer cell line) to model lipid accumulation. STE and its key component, oleanolic acid, significantly reduced intracellular levels of TG, TC, LDL-C, and the number of lipid droplets. Western blot analysis revealed that these effects were mediated by the AMPK-SREBP1 pathway, involving key proteins such as p-AMPK, SREBP1, FAS, ACC, and SCD. The AMPK (AMP-activated protein kinase) pathway plays a critical role in cellular energy homeostasis and can influence inflammation[3]. Activation of AMPK has been shown to regulate lipid metabolism by inhibiting SREBP1 (sterol regulatory element-binding protein 1), a key transcription factor involved in lipid biosynthesis. This pathway's regulation helps reduce lipid accumulation and inflammation, which are central to NAFLD progression. Previous studies have demonstrated that AMPK activation can modulate inflammatory responses and lipid metabolism, which are crucial in NAFLD development[2][3]. The current study builds on these findings by demonstrating that STE can effectively activate the AMPK pathway, thereby reducing lipid accumulation and improving liver function in NAFLD models. Additionally, the study highlighted the role of oxidative stress and inflammation in NAFLD progression. Prior research indicated that oxidative stress and inflammation are significant contributors to liver damage in NAFLD[2][4]. The current study's findings align with this, as STE treatment also reduced markers of oxidative stress and inflammation, further supporting its therapeutic potential. In conclusion, the study by Qinghai University confirmed that sea buckthorn triterpenoid acid enrichment (STE) can improve NAFLD by regulating the AMPK-SREBP1 pathway, reducing lipid accumulation, and alleviating oxidative stress and inflammation. These findings offer promising insights into new therapeutic strategies for managing NAFLD, potentially benefiting millions of individuals affected by this condition.

MedicineHealthBiochem

References

Main Study

1) Exploring the effect and mechanism of Hippophae rhamnoides L. triterpenoid acids on improving NAFLD based on network pharmacology and experimental validation in vivo and in vitro.

Published 8th August, 2024

https://doi.org/10.1016/j.jep.2024.118657

Related Studies

2) Molecular pathways of nonalcoholic fatty liver disease development and progression.

https://doi.org/10.1007/s00018-018-2947-0

3) AICAR induces cyclooxygenase-2 expression through AMP-activated protein kinase-transforming growth factor-beta-activated kinase 1-p38 mitogen-activated protein kinase signaling pathway.

https://doi.org/10.1016/j.bcp.2010.06.049

4) Triterpenoid-rich fraction from Ilex hainanensis Merr. attenuates non-alcoholic fatty liver disease induced by high fat diet in rats.

https://doi.org/10.1142/S0192415X13500353


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