Abstract
Excessive reactive oxygen species (ROS) promotes the oxidative stress of keratinocytes, eventually causing cell damage. The natural bromophenol bis (2,3,6-tribromo-4,5-dihydroxybenzyl) ether (BTDE) from marine red algae has been reported to have a varied bioactivity; however, its antioxidant effect has yet to be investigated systemically. Our present work aimed to explore the antioxidant effect of BTDE both on the molecular and cellular models and also to illustrate the antioxidant mechanisms. Our results showed that BTDE could effectively scavenge ABTS free radicals and protect HaCaT cells from damage induced by H2O2. Mechanism studies in HaCaT cells demonstrated that BTDE attenuated hydrogen peroxide (H2O2)-induced ROS production, reduced the malondialdehyde (MDA) level, decreased the oxidized glutathione (GSSG)/glutathione (GSH) ratio, and increased the antioxidant enzyme superoxide dismutase (SOD). Moreover, BTDE could inhibit the expression of Kelch-like epichlorohydrin-associated protein 1 (Keap1) and increase the expression of both nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream proteins TrXR1, HO-1, and NQO1. BTDE also activated the upstream signaling pathway of Nrf2 such as AKT pathway, while not activating the ERK or AMPKα pathways. In general, BTDE is a promising antioxidant to protect HaCaT cells against oxidative damage via Nrf2-mediated pathways.
Highlights
Reactive oxygen species (ROS) are produced in the process of physiologic activity and are necessary for the basic biological processes of keratinocytes, such as proliferation and differentiation [1]
The results showed that BTDE obviously scavenged in vitro ABTS free radicals (Figure 1b), suggesting its antioxidant activity
Since nuclear factor erythroid 2-related factor 2 (Nrf2) plays an important role in confronting cellular oxidative stress, we investigated the effect of BTDE on Nrf2 expression in HaCaT cells
Summary
Reactive oxygen species (ROS) are produced in the process of physiologic activity and are necessary for the basic biological processes of keratinocytes, such as proliferation and differentiation [1]. The excessive production of cellular ROS may attenuate the skin’s antioxidant system and cause oxidative damage, atopic dermatitis, premature skin aging, skin cancer, and other diseases [2]. There are no clinical drugs for the treatment of skin oxidative damage. It is believed that both exogenous and endogenous oxidative stress lead to the excessive production of ROS in keratinocytes. The balance between the ROS production and its elimination maintains the skin redox balance [3,4,5]. Removal of excessive ROS and stimulating cellular response to ROS have positive significance for the treatment of the aforementioned skin diseases
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