ArticleCell & bioscience2019
BabaoDan attenuates high-fat diet-induced non-alcoholic fatty liver disease via activation of AMPK signaling.
Article in Cell & bioscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 100 citations in OpenAlex.
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- Fortunellin Elevates the AMPK Pathway to Reduce Lipid Deposition and Immune Disorders in Young Non-Alcoholic Fatty Liver Disease RatsEndocrine, metabolic & immune disorders drug targets · 2026Article
- Research Progress on the Mechanisms of Traditional Chinese Medicine in Preventing and Treating HCC Invasion and Metastasis Based on Lipid Metabolic Reprogramming.Current topics in medicinal chemistry · 2026Review
- The triad of maternal gut-breast milk-infant gut microbial transmission in early life as a critical pathway for microbial inheritance.Gut microbes · 2025Article
- Licochalcone A ameliorates lipid accumulation in metabolic dysfunction-associated steatotic liver disease via upregulating PPARα/CPT1α.Histology and histopathology · 2025Article
- Effect of Ningxiang pig-derived Lactobacillus reuteri supplementation on the growth performance, lipid metabolism, and gut microbiota of finishing pigs.Porcine health management · 2025Article
- UPLC-MS/MS Metabolomics Reveals Babao Dan's Mechanisms in MASH Treatment with Integrating Network Pharmacology and Molecular Docking.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Rhein alleviates hepatic steatosis in NAFLD mice by activating the AMPK/ACC/SREBP1 pathway to enhance lipid metabolism.Molecular medicine (Cambridge, Mass.) · 2025Article
- Naringin ameliorates high-fat diet-induced hepatotoxicity and dyslipidemia in experimental rat model via modulation of anti-oxidant enzymes, AMPK and SERBP-1c signaling pathways.Toxicology reports · 2025Article
- Differences in Fatty Acid Metabolism between MCDD and HFD Induced Metabolic Dysfunction-associated Fatty Liver Disease Model Mice.Biological procedures online · 2025Article
- ILF3 inhibits p-AMPK expression to drive non-alcoholic fatty liver disease progression.World journal of hepatology · 2025Article
- IREB2 Knockdown Alleviates High-Fat Diet-Induced Nonalcoholic Fatty Liver Disease by TLR4/NF-κB Signaling Inactivation.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2025Article
- Targeting AMPK related signaling pathways: A feasible approach for natural herbal medicines to intervene non-alcoholic fatty liver disease.Journal of pharmaceutical analysis · 2025Review
- Leonurine Inhibits Hepatic Lipid Synthesis to Ameliorate NAFLD via the ADRA1a/AMPK/SCD1 Axis.International journal of molecular sciences · 2024Article
- Fanlian Huazhuo Formula alleviates high-fat diet-induced non-alcoholic fatty liver disease by modulating autophagy and lipid synthesis signaling pathway.World journal of gastroenterology · 2024Article
- Lactucopicrin promotes fatty acid β-oxidation and attenuates lipid accumulation through adenosine monophosphate-activated protein kinase activation in free fatty acid-induced human hepatoblastoma cancer cells.Food science & nutrition · 2024Article
- Cytokine Storm in COVID-19: Insight into Pathological Mechanisms and Therapeutic Benefits of Chinese Herbal Medicines.Medicines (Basel, Switzerland) · 2024Review
- Early and long-term responses of intestinal microbiota and metabolites toBMC medicine · 2024Article
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBabaodan (BBD), a traditional Chinese medicine, has been shown to have protective effects during liver injury and ameliorate liver disease progression, but little is known about its effect on non-alcoholic fatty liver disease (NAFLD). The aim of this study was to investigate the effects of BBD on obesity-induced NAFLD.
methodsC57BL/6 J mice were fed with normal diet, high fat diet (HFD) or HFD + BBD for 8 weeks. Weights of all mice were recorded every 3 days. At the end of the experiments, the level of livers, kidneys and adipose tissues of each animal was weighed. Blood serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C) cholesterol, low density lipoprotein cholesterol (LDL-C), glucose and leptin were detected with appropriate test kits. Haematoxylin-eosin (HE), Masson trichrome and Oil Red O staining of the liver were performed. We applied immunohistochemical analysis to investigate the expression of TNF-α, IL-6 and leptin in liver tissue. The expression of genes related lipid anabolism (SREBP1-c, ACC, SCD-1, LXRα and CD36) and ß-oxidation (CPT-1 and PPARα) in liver and adipose tissues was determined by RT-PCR. The expression of AMPK and p-AMPK was determined by western blot analysis.
resultsWe found the weight of bodies and tissues (retroperitoneal fat pads, kidneys and livers) of mice fed with HFD + BBD were significantly lower than that of HFD-fed mice. And liver injury induced by HFD was relieved in mice treated with BBD, accompanied with significant reduction were observed in serum ALT/AST activities and alleviated pathological damage. The levels of glucose, TG, TC, HDL-C and LDL-C in the liver or serum were significantly decreased on HFD + BBD group compared with HFD group. Furthermore, BBD treatment reduced the level of TNF-α and IL-6 induced by HFD. The level of leptin in the liver and serum were reduced in mice fed with HFD + BBD than that of HFD-fed mice. Several lipid synthesis genes (SREBP1-c, ACC, SCD-1, LXRα and CD36) were down-regulated and that of ß-oxidation (CPT-1 and PPARα) up-regulated in HFD + BBD group compared with HFD group. In addition, BBD increased the expression of p-AMPK compared with untreated HFD group, which suggested BBD improved the activation of AMPK pathway.
conclusionIn summary, our results indicate that BBD has potential applications in the prevention and treatment of NAFLD, which may be closely related to its effect on lipid metabolism via activation of AMPK signaling.
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