Alleviation of Liver Dysfunction, Oxidative Stress and Inflammation Underlies the Protective Effect of Ferulic Acid in Methotrexate-Induced Hepatotoxicity

In multiple studies, involvement of oxidative stress in the pathogenesis of methotrexate (MTX)-mediated liver damage has been confirmed. Use of many drugs has been examined experimentally in order to prevent or diminish oxidative stress. However, no study has yet examined the effects of ferulic acid...

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Bibliographic Details
Published in:	Drug design, development and therapy Vol. 14; pp. 1933 - 1941
Main Authors:	Roghani, Mozhdeh, Kalantari, Heibatullah, Khodayar, Mohammad Javad, Khorsandi, Layasadat, Kalantar, Mojtaba, Goudarzi, Mehdi, Kalantar, Hadi
Format:	Journal Article
Language:	English
Published:	New Zealand Dove Medical Press Limited 01-01-2020 Dove Dove Medical Press
Subjects:	Administration, Oral Animals Antioxidants (Nutrients) Coumaric Acids - administration & dosage Coumaric Acids - pharmacology Dose-Response Relationship, Drug ferulic acid Inflammation Inflammation - drug therapy Inflammation - metabolism Injections, Intraperitoneal Interleukins Liver Liver - drug effects Liver - metabolism Liver diseases Liver Diseases - drug therapy Liver Diseases - metabolism Male Methotrexate Methotrexate - administration & dosage Methotrexate - antagonists & inhibitors Methotrexate - pharmacology Mice Nitric oxide Original Research oxidative damage Oxidative stress Oxidative Stress - drug effects Protective Agents Structure-Activity Relationship Superoxides Iran methotrexate oxidative damage ferulic acid inflammation mice
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Summary:	In multiple studies, involvement of oxidative stress in the pathogenesis of methotrexate (MTX)-mediated liver damage has been confirmed. Use of many drugs has been examined experimentally in order to prevent or diminish oxidative stress. However, no study has yet examined the effects of ferulic acid (FA) on MTX-induced liver damage. This study aimed at evaluating the effects of FA on protection against liver damage induced by MTX in mice. In this the mice were divided into five groups in a random manner: I) control; II) MTX (20 mg/kg); III and IV) FA (50 and 100 mg/kg) + MTX; and V) FA (100 mg/kg), and we measured serum factors, oxidative stress and inflammatory factors. In the MTX group, accumulation of inflammatory cells, accumulation of red blood cell (RBC), and nuclear pyknosis (NP) were detected in the liver. In line with the histological data, the levels of nitric oxide (NO), malondialdehyde (MDA), interleukin-6 (IL-6), and tumor necrosis factor-α increased (TNF-α), whereas the reduced glutathione (GSH), catalase (CAT), total antioxidant capacity (TAC), superoxide dismutase (SOD), and glutathione peroxidase (GPx) content reduced in the MTX group. However, FA ameliorated these hazardous effects in the antioxidant and anti-inflammatory systems in MTX-treated groups. Based on our findings, oxidative stress impairment and MTX-induced liver damage were ameliorated following FA pretreatment at both histological and biochemical levels. Therefore, FA can be effectively used in abrogation of MTX-induced toxicity.
ISSN:	1177-8881 1177-8881
DOI:	10.2147/DDDT.S237107