ArticleActa pharmacologica Sinica2017
Astragaloside IV attenuates free fatty acid-induced ER stress and lipid accumulation in hepatocytes via AMPK activation.
Article in Acta pharmacologica Sinica, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.
- Evaluation of fatty liver disease self-care applications: a systematic review and evaluation of apps using the mobile application rating scale (MARS).BMC gastroenterology · 2026Pooled it
- Protective effects of Astragaloside IV on various liver diseases: From chemistry to herbal medicines (Review).International journal of molecular medicine · 2026Review
- Review
- Systematic investigation of the potential multi-target pharmacological mechanisms of Astragaloside IV in polycystic ovary syndrome via network pharmacology and in vivo/in vitro experiments.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Computational proteome-wide screening reveals potential targets of astragaloside IV inFrontiers in veterinary science · 2026Article
- Astragaloside IV in hepatocellular carcinoma: repolarizing macrophages to reprogram the tumor microenvironment.Frontiers in pharmacology · 2026Review
- Astragaloside IV reduces diabetic kidney injury by inhibiting the PKC/NOX4/MAPK pathway.Renal failure · 2025Article
- Article
- Research Progress and Prospects of Saponins in the Treatment of NAFLD: A Narrative Review.Molecules (Basel, Switzerland) · 2025Review
- Research Progress on Chemical Components ofMolecules (Basel, Switzerland) · 2025Review
- Astragaloside IV alleviates septic myocardial injury through DUSP1-Prohibitin 2 mediated mitochondrial quality control and ER-autophagy.Journal of advanced research · 2025Article
- Astragaloside IV as a promising therapeutic agent for liver diseases: current landscape and future perspectives.Frontiers in pharmacology · 2025Review
- Therapeutic potential and mechanistic insights of astragaloside IV in the treatment of arrhythmia: a comprehensive review.Frontiers in pharmacology · 2025Review
- Heat shock proteins (HSPs) in non-alcoholic fatty liver disease (NAFLD): from molecular mechanisms to therapeutic avenues.Biomarker research · 2024Review
- Exploring the immunometabolic potential of Danggui Buxue Decoction for the treatment of IBD-related colorectal cancer.Chinese medicine · 2024Review
- Regulation and targeting of SREBP-1 in hepatocellular carcinoma.Cancer metastasis reviews · 2024Review
- Pin1 Exacerbates Non-Alcoholic Fatty Liver Disease by Enhancing Its Activity through Binding to ACC1.International journal of molecular sciences · 2024Article
- Review
- Could Cyclosiversioside F Serve as a Dietary Supplement to Prevent Obesity and Relevant Disorders?International journal of molecular sciences · 2023Review
- Effect of Isoquercitrin on Free Fatty Acid-Induced Lipid Accumulation in HepG2 Cells.Molecules (Basel, Switzerland) · 2023Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the pathogenesis of non-alcoholic fatty liver disease (NAFLD) is not completely understood, the increased influx of free fatty acids (FFAs) into the liver and the FFA-induced hepatic endoplasmic reticulum (ER) stress are two crucial pathogenic processes in the initiation and development of NAFLD. In this study we investigated the effects of astragaloside IV (AS-IV), a bioactive compound purified from Astragali Radix, on FFA-induced lipid accumulation in hepatocytes and elucidated the underlying mechanisms. Human HepG2 cells and primary murine hepatocytes were exposed to FFAs (1 mmol/L, oleate/palmitate, 2:1 ratio) with or without AS-IV for 24 h. Exposure to FFAs induced marked lipid accumulation in hepatocytes, whereas co-treatment with AS-IV (100 μg/mL) significantly attenuated this phenomenon. Notably, AS-IV (50-200 μg/mL) concentration-dependently enhanced the phosphorylation of AMPK, acetyl-CoA carboxylase (ACC) and SREBP-1c, inhibited the accumulation and nuclear translocation of mature SREBP-1 and subsequently decreased the mRNA levels of lipogenic genes including acc1, fas and scd1. AS-IV treatment also concentration-dependently attenuated FFA-induced hepatic ER stress evidenced by the reduction of the key markers, GRP78, CHOP and p-PERK. Pretreated the cells with the AMPK inhibitor compound C (20 μmol/L) greatly diminished these beneficial effects of AS-IV. Our results demonstrate that AS-IV attenuates FFA-induced ER stress and lipid accumulation in an AMPK-dependent manner in hepatocytes, which supports its use as promising therapeutics for hepatic steatosis.
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