ArticleMolecular medicine reports2017
Licochalcone E protects against carbon tetrachloride‑induced liver toxicity by activating peroxisome proliferator-activated receptor gamma.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- Licochalcone E Ameliorates Hepatic Steatosis in Obese Mice by Activating the Sirt1/AMPK Pathway and Reducing Hepatic Lipid Accumulation.Biomolecules & therapeutics · 2026Article
- Chalcones as Multi-target Ligands for Alzheimer's Disease: A Review of Synthetic Strategies and Therapeutic Promise.Mini reviews in medicinal chemistry · 2026Review
- Natural Chalcones in Chinese Materia Medica: Licorice.Evidence-based complementary and alternative medicine : eCAM · 2020Review
- Hepatoprotective activity of raspberry ketone is mediatedToxicology research · 2019Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to investigate the hepatoprotective role of Licochalcone E (LCE) and its mechanism of action in a mouse model of carbon tetrachloride (CCl4)‑induced liver toxicity. Hepatotoxicity was induced in Kunming mice via an intraperitoneal injection (IP) of CCl4, 10 ml/kg body weight, diluted with corn oil at a 1:500 ratio. LCE was administered once a day for 7 days (IP) as pretreatment at a dose of 5 mg/kg/day. The levels of C‑reactive protein (CRP) and tumor necrosis factor (TNF)‑α were analyzed to determine the inflammation status. The levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were analyzed using ELISA assays. Liver ultrastructure was observed via optical microscopy. The mRNA and protein expression levels of peroxisome proliferator‑activated receptor (PPAR)γ, and nuclear factor (NF)‑κB were assayed using quantitative polymerase chain reaction and western blot analysis, respectively. Pretreatment with LCE decreased levels of ALT, AST, CRP and TNF‑α, and NF‑κB expression in the experimental hepatotoxicity mice model induced by CCl4. In addition, LCE increased the expression of PPARγ and normalized the hepatic histoarchitecture. However, the effects of LCE were reversed by cotreatment with the PPARγ inhibitor GW9662. The present study suggests that LCE may be used for the treatment of hepatotoxicity, and primarily exhibits its protective role through a PPARγ/NF‑κB‑mediated pathway.
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Registered trials
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