Abstract
Objective: To investigate the hepatoprotective mechanisms of taxifolin in mice with acute liver injury induced by CCl4. Methods: ICR (Institute of Cancer research) mice were orally pretreated using taxifolin for 7 consecutive days and were then given single intraperitoneal (i.p.) injections of 0.2% CCl4 (10 mL/kg body weight, i.p.). Liver injury was then determined using assays of serum alanine aminotransferase (sALT) and serum aspartate aminotransferase (sAST). Further, to investigate the hepatoprotective mechanisms of taxifolin, we determined malondialdehyde (MDA) levels and superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione reductase (GRd) activities. Results: CCl4-induced liver injury led to significant increases in sALT and sAST activities, and these increases were limited by taxifolin and silymarin (Sily) pretreatments. Histological analyses also indicated that taxifolin and Sily decreased the range of liver lesions in CCl4-treated mice and vacuole formation, neutrophil infiltration, and necrosis were visibly reduced. In addition, SOD, GPx, and GRd activities were increased and MDA levels were decreased after taxifolin and Sily treatments. Conclusion: The hepatoprotective mechanisms of taxifolin and Sily are related to decreases in MDA levels presumably due to increased antioxidant enzyme activities. These outcomes suggest that taxifolin mitigates acute liver injury resulted from CCl4 in mice, demonstrating the hepatoprotective effects of taxifolin.
Highlights
The formation and degradation of reactive oxygen species (ROS) in all aerobic organisms is commonly known; further, ROS mediate various intracellular signaling cascades [1]
These outcomes suggest that taxifolin mitigates acute liver injury resulted from CCl4 in mice, demonstrating the hepatoprotective effects of taxifolin
CCl4 treatments significantly increased the activities of serum alanine aminotransferase (sALT) and serum aspartate aminotransferase (sAST)
Summary
The formation and degradation of reactive oxygen species (ROS) in all aerobic organisms is commonly known; further, ROS mediate various intracellular signaling cascades [1]. The excessive production of ROS induces oxidative stress in human bodies, causing damage to proteins, DNA, and lipids and leading to degenerative and pathological disease states [2]. Some environmental factors, such as cigarette smoke and certain drugs, can increase free radical activities in the liver. The liver plays an essential role in various metabolic processes; liver injury leads to various severe morbidities. Various toxic chemicals and drugs and infection with viruses, such as hepatitis, cause liver injury [4]. Carbon tetrachloride (CCl4 ) metabolism via cytochrome P450 leads to Nutrients 2019, 11, 2655; doi:10.3390/nu11112655 www.mdpi.com/journal/nutrients
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
