Fucoxanthin Exerts Cytoprotective Effects against Hydrogen Peroxide-induced Oxidative Damage in L02 Cells.

Xia Wang,Shun-Mei Liu,Tian-Liang Zhang,Min Cheng,Yan-Jun Cui,Min-Min Zhu,Jia Qi,Guang-Ce Wang

doi:10.1155/2018/1085073

Abstract

Several previous studies have demonstrated the excellent antioxidant activity of fucoxanthin against oxidative stress which is closely related to the pathogenesis of liver diseases. The present work was to investigate whether fucoxanthin could protect human hepatic L02 cells against hydrogen peroxide- (H2O2-) induced oxidative damage. Its effects on H2O2-induced cell viability, lactate dehydrogenase (LDH) leakage, intracellular reduced glutathione, and reactive oxygen species (ROS) contents, along with mRNA and protein relative levels of the cytoprotective genes including Nrf2, HO-1, and NQO1, were investigated. The results showed that fucoxanthin could upregulate the mRNA and protein levels of the cytoprotective genes and promote the nuclear translocation of Nrf2, which could be inhibited by the PI3K inhibitor of LY294002. Pretreatment of fucoxanthin resulted in decreased LDH leakage and intracellular ROS content but enhanced intracellular reduced glutathione. Interestingly, pretreatment using fucoxanthin protected against the oxidative damage in a nonconcentration-dependent manner, with fucoxanthin of 5 μM demonstrating the optimal effects. The results suggest that fucoxanthin exerts cytoprotective effects against H2O2-induced oxidative damage in L02 cells, which may be through the PI3K-dependent activation of Nrf2 signaling.

Highlights

Reactive oxygen species (ROS), including free radical such as hydroxyl radical and non-free radical such as hydrogen peroxide (H2 O2 ), are highly reactive byproducts derived from normal cell metabolism, especially from that of mitochondria
L02 cells were treated with H2 O2 at different concentrations (100, 200, 400, 600, 800, 1000, 1200, and 1600 μM, respectively) and the appropriate concentration used to induce oxidative damage was evaluated by MTT assay
H2 O2 physiologically exists in living cells where it can act as a cellular signal transducer below the concentration of 1 μM, at higher concentrations it might result in adverse effects such as growth arrest or cell death caused by the derived oxidative stress [28]

Summary

Introduction

Reactive oxygen species (ROS), including free radical such as hydroxyl radical and non-free radical such as hydrogen peroxide (H2 O2 ), are highly reactive byproducts derived from normal cell metabolism, especially from that of mitochondria [1]. Hepatic cells are rich in mitochondria and prone to generate ROS [5]. Role of oxidative damage in the pathogenesis of various liver injuries has been confirmed. It has been suggested that the overproduction of H2 O2 contributes to the pathogenesis of many liver diseases such as hepatitis C virus infection, cholestasis and Wilson’s disease etc [6]. Enzymatic antioxidants (such as glutathione (GSH) or glutathionerelated enzyme system) and non-enzymatic ones are the two major systems to control ROS generation and counteract the oxidative damage [7]. It has become an interesting and urgent topic for researchers to find excellent antioxidants for the prevention of liver diseases

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Conclusion