ArticlePloS one2014
The protective effect of Esculentoside A on experimental acute liver injury in mice.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 65 citations in OpenAlex.
- Animal models accurately representing acute liver failure (Review).International journal of molecular medicine · 2026Review
- Resolvin D1 values in patients with alcohol-associated liver disease.BMC gastroenterology · 2025Article
- Hesperidin alleviated D-GalN/LPS induced acute liver injury in mice: insights into gut microbiota and the Nrf2/Keap1 pathway.Frontiers in microbiology · 2025Article
- Therapeutic potential of oleanolic acid in liver diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Naringenin Prevents Oxidative Stress and Inflammation in LPS-Induced Liver Injury through the Regulation of LncRNA-mRNA in Male Mice.Molecules (Basel, Switzerland) · 2022Article
- Esculentoside A could attenuate apoptosis and inflammation in TNBS-induced ulcerative colitis via inhibiting the nuclear translocation of NF-κB.Annals of translational medicine · 2022Article
- A potential antiviral activity of Esculentoside A against binding interactions of SARS-COV-2 spike protein and angiotensin converting enzyme 2 (ACE2).International journal of biological macromolecules · 2021Article
- Prophylactic and therapeutic roles of oleanolic acid and its derivatives in several diseases.World journal of clinical cases · 2020Review
- Spontaneous evolution of human skin fibroblasts into wound-healing keratinocyte-like cells.Theranostics · 2019Article
- Downregulation of Glt25d1 aggravates carbon tetrachloride‑induced acute hepatic injury through activation of the TGF‑β1/Smad2 signaling pathway.Molecular medicine reports · 2018Article
- Plasmon-activated water effectively relieves hepatic oxidative damage resulting from chronic sleep deprivation.RSC advances · 2018Article
- Hepatoprotective effect of methyl ferulic acid against carbon tetrachloride-induced acute liver injury in rats.Experimental and therapeutic medicine · 2018Article
- Cytochrome P450 1A1 and 1B1 promoter CpG island methylation regulates rat liver injury induced by isoniazid.Molecular medicine reports · 2018Article
- The Pharmacological Targets and Clinical Evidence of Natural Products With Anti-hepatic Inflammatory Properties.Frontiers in pharmacology · 2018Review
- Esculentoside A ameliorates cecal ligation and puncture-induced acute kidney injury in rats.Experimental animals · 2017Article
- Protective effect of human serum amyloid P on CCl4-induced acute liver injury in mice.International journal of molecular medicine · 2017Article
- Hydrostatin-SN1, a Sea Snake-Derived Bioactive Peptide, Reduces Inflammation in a Mouse Model of Acute Lung Injury.Frontiers in pharmacology · 2017Article
- Effect of mild hypothermia preconditioning against low temperature (4°C) induced rat liver cell injury in vitro.PloS one · 2017Article
- Kampo formula "Hochu-ekki-to" suppressed carbon tetrachloride-induced hepatotoxicity in mice.Environmental health and preventive medicine · 2016Article
- Sasa veitchii extract suppresses carbon tetrachloride-induced hepato- and nephrotoxicity in mice.Environmental health and preventive medicine · 2016Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory response and oxidative stress are considered to play an important role in the development of acute liver injury induced by carbon tetrachloride (CCl4) and galactosamine (GalN)/lipopolysaccharides (LPS). Esculentoside A (EsA), isolated from the Chinese herb phytolacca esculenta, has the effect of modulating immune response, cell proliferation and apoptosis as well as anti-inflammatory effects. The present study is to evaluate the protective effect of EsA on CCl4 and GalN/LPS-induced acute liver injury. In vitro, CCK-8 assays showed that EsA had no cytotoxicity, while it significantly reduced levels of TNF-α and cell death rate challenged by CCl4. Moreover, EsA treatment up-regulated PPAR-γ expression of LO2 cells and reduced levels of reactive oxygen species (ROS) challenged by CCl4. In vivo, EsA prevented mice from CCl4-induced liver histopathological damage. In addition, levels of AST and ALT were significantly decreased by EsA treatment. Furthermore, the mice treated with EsA had a lower level of TNF-α, Interleukin (IL)-1β and IL-6 in mRNA expression. EsA prevented MDA release and increased GSH-Px activity in liver tissues. Immunohistochemical staining showed that over-expression of F4/80 and CD11b were markedly inhibited by EsA. The western bolt results showed that EsA significantly inhibited CCl4-induced phosphonated IkBalpha (P-IκB) and ERK. Furthermore, EsA treatment also alleviated GalN/LPS-induced acute liver injury on liver enzyme and histopathological damage. Unfortunately, our results exhibited that EsA had no effects on CCl4-induced hepatocyte apoptosis which were showed by TUNEL staining and Bax, Caspase-3 and cleaved Caspase-3 expression. Our results proved that EsA treatment attenuated CCl4 and GalN/LPS-induced acute liver injury in mice and its protective effects might be involved in inhibiting inflammatory response and oxidative stress, but not apoptosis with its underlying mechanism associated with PPAR-γ, NF-κB and ERK signal pathways.
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