Abstract
ABSTRACTObjective: We aimed to investigate the effect of Sicyos angulatus (SA) ethanolic extracts as antioxidants and potential treatments for liver disease.Methods: To establish a mouse model of liver injury, C57BL/6 male mice were injected via the caudal vein with a single dose of concanavalin A (Con A, 15 mg kg−1). SA extracts were administered once by oral gavage 30 min before Con A injection.Results: In vitro studies showed that SA decreased tert-butyl hydroperoxide (t-BHP)-induced reactive oxygen species (ROS) production. SA administration reduced plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, as well as hepatic ROS levels, in a dose-dependent manner. Moreover, SA increased the activities of the hepatic antioxidant enzymes superoxide dismutase, catalase, and glutathione peroxidase in a dose-dependent manner. Furthermore, SA treatment reduced pro-apoptotic protein levels. Con A-mediated cytosolic release of Smac/DIABLO and apoptosis-inducing factor (AIF), which are markers of necrosis, were dramatically decreased in HepG2 cells treated with SA.Conclusion: SA ameliorated liver injury and might be a good strategy for the treatment of liver injury.
Highlights
The liver is a major organ that is exposed to bacterial products, toxins, and food-derived antigens [1]
These results suggested that the Sicyos angulatus (SA) extract exerted a potent antioxidant activity in vitro and in vivo and attenuated liver injury in Con A-induced animal models
We investigated the effect of SA as a potent candidate for the treatment of liver injury
Summary
The liver is a major organ that is exposed to bacterial products, toxins, and food-derived antigens [1]. Reactive oxygen species (ROS) oxidize cellular proteins, lipids, and nucleic acids, which leads to general cellular damage and dysfunction and may initiate cell death through various signaling cascades [3]. ROS generation is a major factor in the pathogenesis of many liver diseases [4,5]. Hepatocytic protein, lipid, and DNA are primarily affected by ROS, resulting in functional abnormalities in the liver [6]. Its excessive activation is known to induce liver damage by increasing the production of cytokines, such as tumor necrosis factor-alpha (TNFα) [7]. Liver injury induced by TNF-α has been proposed to involve the generation of ROS derived from either mitochondrial or non-mitochondrial sources [8]. Antioxidant therapy alone or in combination with other strategies appears to be a potential treatment for various liver diseases
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
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 call
