Oxidative stress induced by the overproduction of free radicals or reactive oxygen species (ROS) has been considered as a key pathogenic mechanism contributing to the initiation and progression of injury in liver diseases. Consequently, during the last few years antioxidant substances, such as superoxide dismutase (SOD), resveratrol, colchicine, eugenol, and vitamins E and C have received increasing interest as potential therapeutic agents in chronic liver diseases. These substances have demonstrated their efficacy in equilibrating hepatic ROS metabolism and thereby improving liver functionality. However, many of these agents have not successfully passed the scrutiny of clinical trials for the prevention and treatment of various diseases, mainly due to their unspecificity and consequent uncontrolled side effects, since a minimal level of ROS is needed for normal functioning. Recently, cerium oxide nanoparticles (CeONPs) have emerged as a new powerful antioxidant agent with therapeutic properties in experimental liver disease. CeONPs have been reported to act as a ROS and reactive nitrogen species (RNS) scavenger and to have multi-enzyme mimetic activity, including SOD activity (deprotionation of superoxide anion into oxygen and hydrogen peroxide), catalase activity (conversion of hydrogen peroxide into oxygen and water), and peroxidase activity (reducing hydrogen peroxide into hydroxyl radicals). Consequently, the beneficial effects of CeONPs treatment have been reported in many different medical fields other than hepatology, including neurology, ophthalmology, cardiology, and oncology. Unlike other antioxidants, CeONPs are only active at pathogenic levels of ROS, being inert and innocuous in healthy cells. In the current article, we review the potential of CeONPs in several experimental models of liver disease and their safety as a therapeutic agent in humans as well.
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http://dx.doi.org/10.3390/antiox10050660 | DOI Listing |
J Transl Med
January 2025
Maimonides Biomedical Research Institute of Cordoba (IMIBIC), University of Cordoba, Cordoba, Spain.
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View Article and Find Full Text PDFBMC Complement Med Ther
January 2025
Department of Nutrition, Qazvin University of Medical Sciences, Qazvin, Iran.
Background: It seems that oxidative stress is involved in the occurrence and progression of non-alcoholic fatty liver disease (NAFLD). Considering the antioxidant features of Ellagic acid (EA), this study was designed to assess the effect of EA on some biochemical factors in patients with NAFLD.
Methods: In this clinical trial, 44 patients were selected based on including criteria and randomly received 180 mg of EA per day (n = 22) or placebo (n = 22) for 8 weeks.
BMC Gastroenterol
January 2025
Center for General Practice Medicine, Department of Infectious Diseases, Zhejiang Provincial People's Hospital (Affiliated People's Hospital, Hangzhou Medical College), Hangzhou, Zhejiang, China.
Background: Neuregulin (NRG) family is involved in energy metabolism, among which NRG1 is a neuregulin proved to play a protective role in MAFLD cells. But the presice echanism has not been fully illustrated. This study aimed to investigate the role of NRG1 via the ERK/SIRT1 signaling in the pathogenesis of MAFLD.
View Article and Find Full Text PDFSci Rep
January 2025
Shaoxing Maternity and Child Health Care Hospital, No. 222 Fenglin East Road, Shaoxing, 312000, Zhejiang, China.
Pediatric non-alcoholic fatty liver disease (NAFLD) is emerging as a worldwide health concern with the potential to advance to cirrhosis and liver cancer. NAFLD can also directly contribute to heart problems through inflammation and insulin resistance, even in individuals without other risk factors. The pathological mechanisms of NAFLD are linked to functional differences of miRNAs in different biological environments.
View Article and Find Full Text PDFCell Mol Gastroenterol Hepatol
January 2025
Department of Medicine, University of Western Ontario, London, Ontario N6A 5W9, Canada; Verspeeten Family Cancer Centre, London Health Sciences Centre, London, Ontario, Canada. Electronic address:
Background And Aims: Loss of the tumor suppressor gene Apc in Lgr5+ intestinal stem cells results in aberrant Wnt signaling and colonic tumorigenesis. In the setting of injury, however, we and others have also shown that non-stem cells can also give rise to colonic tumors. The mechanism by which inflammation leads to cellular plasticity and cancer, however, remains largely unknown.
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