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Open AccessArticle

Floridoside Exhibits Antioxidant Properties by Activating HO-1 Expression via p38/ERK MAPK Pathway

State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Agro-products, Ningbo University, Ningbo 315211, China
Author to whom correspondence should be addressed.
Mar. Drugs 2020, 18(2), 105;
Received: 10 January 2020 / Revised: 4 February 2020 / Accepted: 8 February 2020 / Published: 10 February 2020
(This article belongs to the Special Issue Marine Natural Product and Oxidative Stress)
Floridoside is a low-molecular-weight organic compound, which can be accumulated by red algae under stressful conditions to protect cells via its excellent antioxidant properties. In the present study, we investigated the antioxidant mechanism of floridoside toward human hepatocyte L-02 cells. We found that floridoside had no toxicity to L-02 cells, and no reactive oxidative species were induced by it either. However, the expression of hemoxygenase-1 (HO-1) protein was up-regulated upon exposure to floridoside, and two antioxidant enzymes, superoxide dismutase (SOD) and GSH-Px, were activated by floridoside. Moreover, we investigated the pathway involved in the production of these antioxidants, p38/extracellular signal-regulated kinase (ERK) MAPK-nuclear factor-erythroid-2-related factor 2 (Nrf2) pathway. ERK1/2 and p38 phosphorylation, nuclear translocation of Nrf2, and activation of ARE luciferase activity were observed upon exposure to floridoside. siRNA interference and inhibitor treatment suppressed the HO-1 expression and the phosphorylation of ERK1/2 and p38, respectively. These results indicated that floridoside exerted its antioxidant activity by activating HO-1 expression via p38/ERK MAPK-Nrf2 pathway in human hepatocyte L-02 cells. View Full-Text
Keywords: floridoside; hepatocyte; antioxidant; Nrf2/HO-1 pathway floridoside; hepatocyte; antioxidant; Nrf2/HO-1 pathway
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Niu, T.; Fu, G.; Zhou, J.; Han, H.; Chen, J.; Wu, W.; Chen, H. Floridoside Exhibits Antioxidant Properties by Activating HO-1 Expression via p38/ERK MAPK Pathway. Mar. Drugs 2020, 18, 105.

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