Abstract

Sargassum species have been reported to be a source of phytochemicals, with a wide range of biological activities. In this study, we evaluated the hepatoprotective effect of a meroterpenoid-rich fraction of the ethanolic extract from Sargassum serratifolium (MES) against tert-butyl hydroperoxide (t-BHP)-treated HepG2 cells. Treatment with MES recovered the cell viability from the t-BHP-induced oxidative damage in a dose-dependent manner. It suppressed the reactive oxygen species production, lipid peroxidation, and glutathione depletion in the t-BHP-treated HepG2 cells. The activity of the antioxidants induced by t-BHP, including superoxide dismutase (SOD) and catalase, was reduced by the MES treatment. Moreover, it increased the nuclear translocation of nuclear factor erythroid 2-related factor 2, leading to the enhanced activity of glutathione S transferase, and the increased production of heme oxygenase-1 and NAD(P)H:quinine oxidoreductase 1 in t-BHP-treated HepG2 cells. These results demonstrate that the antioxidant activity of MES substituted the activity of the SOD and catalase, and induced the production of detoxifying enzymes, indicating that MES might be used as a hepatoprotectant against t-BHP-induced oxidative stress.

Highlights

  • Reactive oxygen species (ROS) are continuously generated in organisms as a by-product of aerobic respiration

  • We investigated the hepatoprotective effect of MES on Tert-butyl hydroperoxide (t-BHP)-treated HepG2 cells, and confirmed that MES induced antioxidants and detoxifying enzymes by activating nuclear factor (erythroid-derived 2)-like 2 (Nrf2)

  • The results demonstrated that MES exhibits a hepatoprotective activity through its intrinsic antioxidant activity and by inducing detoxifying enzymes via the activation of Nrf2 in t-BHP-treated

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Summary

Introduction

Reactive oxygen species (ROS) are continuously generated in organisms as a by-product of aerobic respiration. They play a key physiological role in the stimulation of growth and immune response in living cells in response to intracellular and extracellular stimuli [1]. The ROS level is regulated by enzymatic and non-enzymatic antioxidant defense systems. Excessive ROS are instantly removed by intracellular antioxidant compounds, such as glutathione (GSH), vitamin C, and vitamin E, and are perpetually regulated by antioxidant enzymes, including superoxide dismutase (SOD), catalase, glutathione reductase, glutathione peroxidase, and glutathione S-transferase (GST) [2].

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