Preventive Effect of YGDEY from Tilapia Fish Skin Gelatin Hydrolysates against Alcohol-Induced Damage in HepG2 Cells through ROS-Mediated Signaling Pathways.

Mei-Fang Chen,Fang Gong,Zhong-Ji Qian,Cheng-Yong Li,Chun-Xia Zhou,Sheng-Li Sun,Peng-Zhi Hong,Yuanyuan Zhang

doi:10.3390/nu11020392

Abstract

According to a previous study, YGDEY from tilapia fish skin gelatin hydrolysates has strong free radical scavenging activity. In the present study, the protective effect of YGDEY against oxidative stress induced by ethanol in HepG2 cells was investigated. First, cells were incubated with YGDEY (10, 20, 50, and 100 μM) to assess cytotoxicity, and there was no significant change in cell viability. Next, it was established that YGDEY decreased the production of reactive oxygen species (ROS). Western blot results indicated that YGDEY increased the levels of superoxide dismutase (SOD) and glutathione (GSH) and decreased the expression of gamma-glutamyltransferase (GGT) in HepG2 cells. It was then revealed that YGDEY markedly reduced the expressions of bax and cleaved-caspase-3 (c-caspase-3); inhibited phosphorylation of Akt, IκB-α, p65, and p38; and increased the level of bcl-2. Moreover, the comet assay showed that YGDEY effectively decreased the amount of ethanol-induced DNA damage. Thus, YGDEY protected HepG2 cells from alcohol-induced injury by inhibiting oxidative stress, and this may be associated with the Akt/nuclear factor-κB (NF-κB)/mitogen-activated protein kinase (MAPK) signal transduction pathways. These results demonstrate that YGDEY from tilapia fish skin gelatin hydrolysates protects HepG2 cells from oxidative stress, making it a potential functional food ingredient.

Highlights

Alcohol is primarily metabolized in the liver [1], and the adverse effects of ethanol metabolism have been observed largely [2] through the increased formation of reactive oxygen species (ROS), including the superoxide radical (O2− ), the hydroxyl radical (OH), and hydrogen peroxide (H2 O2 ).During normal metabolic processes, ROS are effectively eliminated by the human body’s antioxidant defense systems, such as the enzymes superoxide dismutase (SOD) and glutathione (GSH) [3].pathological conditions are often associated with oxidative stress in numerous chronic diseases [4]
We investigated the protective effects of YGDEY from tilapia fish skin gelatin hydrolysates against ethanol-induced HepG2 cell injury
The results show that YGDEY could be a novel therapeutic agent against ethanol-induced oxidative stress in HepG2 cells and that its protective effects are related to antioxidant enzymes and AKT/nuclear factor-κB (NF-κB)/mitogen-activated protein kinase (MAPK) signaling pathways

Summary

Introduction

Alcohol is primarily metabolized in the liver [1], and the adverse effects of ethanol metabolism have been observed largely [2] through the increased formation of reactive oxygen species (ROS), including the superoxide radical (O2− ), the hydroxyl radical (OH), and hydrogen peroxide (H2 O2 ).During normal metabolic processes, ROS are effectively eliminated by the human body’s antioxidant defense systems, such as the enzymes superoxide dismutase (SOD) and glutathione (GSH) [3].pathological conditions are often associated with oxidative stress in numerous chronic diseases [4]. Oxidative stress induces lipid peroxidation, apoptosis of hepatocytes, and damage to biological membranes, proteins, and DNA [5]. ALD, a major health problem, is primarily caused by the byproducts of alcohol metabolism, and oxidative stress is a primary causal factor of alcohol-induced liver injury. This is especially the case when the liver has lower levels of antioxidants to counteract the generation of ROS. It has been established that oxidative stress is related to the pathogenesis of ALD, as ROS generation has been observed in alcohol-exposed cultured cells and alcohol-exposed mouse embryos [3]

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