Abstract
Scavenging of oxidative stress by antioxidants may provide a therapeutic strategy for nonalcoholic fatty liver disease (NAFLD). Increasing evidence is supporting the potential application of natural resourced polysaccharides as promising prevention or treatment strategies against NAFLD. In the current study, an acidic heteropolysaccharide, LFP-a1, was isolated and purified from Lycii fructus with successively hot water refluxing extraction, alcohol precipitation, protein removal, and DEAE-52 cellulose chromatographic separation. LFP-a1 was a complicated structured polysaccharide with an average MW of 4.74 × 104 Da and composed of 6 monosaccharides and 1 uronic acid. Preexposure of LFP-a1 could increase the cell viability and reverse the abnormal oxidative stress though inhibition of mitochondrial-mediated apoptotic pathway and correction of cell cycle progression against H2O2 hepatoxicity in NAFLD model L02 cells. Consistently, in vivo study in thioacetamide- (TAA-) induced NAFLD model zebrafish larvae showed LFP-a1 preserved the liver integrity and alleviated TAA-induced oxidative stress through downregulation of abnormal apoptosis. These observations indicated the hepatoprotective activity of LFP-a1, which may be applied for the prevention or treatment of NAFLD or other oxidative stress-related diseases.
Highlights
The conception of oxidative stress basically defines a disturbed condition in which accumulative molecular and/or cellular oxidative injury is observed with the disequilibrium of reactive oxygen species (ROS) generation and in-build antioxidant defensing system [1]
Water soluble deproteinized Lycii fructus polysaccharides (LFPs) were successfully isolated from Lycii fructus powder by a series of procedures including ethanol infusion, water extraction, ethanol precipitation, and deproteination
The improved endogenous antioxidative network enhanced the downstream lipid metabolism, as indicated by the decreased level of MDA. These results clearly indicated the effective protection of LFP-a1 pretreatment against TAA-induced oxidative stress in larval zebrafish nonalcoholic fatty liver disease (NAFLD) model
Summary
The conception of oxidative stress basically defines a disturbed condition in which accumulative molecular and/or cellular oxidative injury is observed with the disequilibrium of reactive oxygen species (ROS) generation and in-build antioxidant defensing system [1]. Repetitive, and/or sustained oxidative stress stems from elevated formation and accumulation of reactive oxygen intermediates (ROI, including free radicals, hydrogen peroxide, hydroxyl radicals, and superoxide anion) have been implicated to be closely interconnected with the initiation and progression of a myriad of pathological lesions which often result in metabolic damage such as aging, cardiovascular diseases, neurological disorders, inflammation, and liver disease. Oxidative stress-mediated toxicity, Oxidative Medicine and Cellular Longevity accompanied by changes in lipid metabolism, gradually destroys the balance between ROS production and detoxification pathways, which further results in feedback overaccumulation of ROS, deficiencies of antioxidant defense, and inevitable impairment of mitochondrial respiratory function in hepatocyte. Previous research has established the protective or therapeutic potency of natural antioxidants upon oxidative injury induced by nonalcoholic insult [4]
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