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Protective effects of ellagic acid against tetrachloride-induced cirrhosis in mice through the inhibition of reactive oxygen species formation and angiogenesis
Ellagic acid has been proven to have anticancer, antimutation, antimicrobial and antiviral functions. The present study investigated whether treatment with ellagic acid was able to prevent tetrachloride (CCl4)-induced cirrhosis through the inhibition of reactive oxygen species (ROS) formation and an...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5639323/ https://www.ncbi.nlm.nih.gov/pubmed/29042921 http://dx.doi.org/10.3892/etm.2017.4966 |
Sumario: | Ellagic acid has been proven to have anticancer, antimutation, antimicrobial and antiviral functions. The present study investigated whether treatment with ellagic acid was able to prevent tetrachloride (CCl4)-induced cirrhosis through the inhibition of reactive oxygen species (ROS) formation and angiogenesis. CCl(4) diluted in olive oil at a final concentration of 10% was used to induce a cirrhosis model. A total of 40 mice were random allocated into four groups, as follows: Control, cirrhosis model, 7.5 mg/kg ellagic acid and 15 mg/kg ellagic acid groups. In the control group, mice were given normal saline. The results indicated that ellagic acid exerted a protective effect, evidently preventing CCl(4)-induced cirrhosis. In addition, treatment with ellagic acid significantly inhibited collagen I and inducible nitric oxide synthase protein expression levels in CCl(4)-induced cirrhosis mice. Oxidative stress and ROS formation were also significantly reduced by ellagic acid treatment. The protein expression levels of vascular endothelial growth factor (VEGF) and VEGF receptor 2 (VEGFR2), and the caspase-3 activity were significantly inhibited by treatment with ellagic acid. In conclusions, these results suggest that ellagic acid exerted protective effects against CCl(4)-induced cirrhosis through the inhibition of ROS formation and angiogenesis. |
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