Abstract
AimOxidative stress has been implicated in the pathogenesis of Nonalcoholic Fatty Liver Disease (NAFLD). Vitamin C and vitamin E are known to react with reactive oxygen species (ROS) blocking the propagation of radical reactions in a wide range of oxidative stress situations. The potential therapeutic efficacy of antioxidants in NAFLD is unknown. The aim of this study was to evaluate the role of antioxidant drugs (vitamin C or vitamin E) in its prevention.MethodsFatty liver disease was induced in Wistar rats by choline-deficient diet for four weeks. The rats were randomly assigned to receive vitamin E (n = 6) – (200 mg/day), vitamin C (n = 6) (30 mg/Kg/day) or vehicle orally.ResultsIn the vehicle and vitamin E-treated rats, there were moderate macro and microvesicular fatty changes in periportal area without inflammatory infiltrate or fibrosis. Scharlach stain that used for a more precise identification of fatty change was strong positive. With vitamin C, there was marked decrease in histological alterations. Essentially, there was no liver steatosis, only hepatocellular ballooning. Scharlach stain was negative. The lucigenin-enhanced luminescence was reduced with vitamin C (1080 ± 330 cpm/mg/minx103) as compared to those Vitamin E and control (2247 ± 790; 2020 ± 407 cpm/mg/minx103, respectively) (p < 0.05). Serum levels of aminotransferases were unaltered by vitamin C or vitamin E.Conclusions1) Vitamin C reduced oxidative stress and markedly inhibited the development of experimental liver steatosis induced by choline-deficient diet ; 2)Vitamin E neither prevented the development of fatty liver nor reduced the oxidative stress in this model.
Highlights
There are evidences that fatty liver, the most common hepatocellular change found in liver biopsies in humans, can play a role in the pathogenesis of chronic liver disease [1,2]
1) Vitamin C reduced oxidative stress and markedly inhibited the development of experimental liver steatosis induced by choline-deficient diet ; 2)Vitamin E neither prevented the development of fatty liver nor reduced the oxidative stress in this model
Some authors have considered that a more accurate denomination for this disease, which encloses the whole spectrum of fatty liver, nonalcoholic steatohepatitis (NASH) and eventually cirrhosis, is Nonalcoholic Fatty Liver Disease (NAFLD) [3,4]
Summary
There are evidences that fatty liver, the most common hepatocellular change found in liver biopsies in humans, can play a role in the pathogenesis of chronic liver disease [1,2]. The current treatment is largely conservative Some hypotheses have been implicated in the pathogenesis of NAFLD, mainly liver injury mediated either by oxidative stress [5,6] or by endotoxins/cytokines [7,8,9]. Hyperinsulinemia [10] Oxidative stress is considered to play a central role in the pathogenesis of NAFLD because the increased production of ROS is known to cause lipid peroxidation, followed by activation of the inflammatory response, and of stellate cells, leading to fibrogenesis [11,12,13]. The aim of this study was to evaluate whether this process can be prevented by antioxidant drugs, vitamin C or vitamin E using an animal model where NAFLD was induced by a choline deficient diet
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.
