Mitochondrial Protection and Anti-inflammatory Effects Induced by Emodin in the Human Neuroblastoma SH-SY5Y Cells Expose
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ORIGINAL PAPER
Mitochondrial Protection and Anti‑inflammatory Effects Induced by Emodin in the Human Neuroblastoma SH‑SY5Y Cells Exposed to Hydrogen Peroxide: Involvement of the AMPK/Nrf2 Signaling Pathway Marcos Roberto de Oliveira1 · Izabel Cristina Custódio de Souza2 · Flávia Bittencourt Brasil3 Received: 23 August 2020 / Revised: 17 October 2020 / Accepted: 12 November 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Emodin (EM; 1,3,8-trihydroxy-6-methylanthracene-9,10-dione; C 15H10O5) is an anthraquinone and exerts cytoprotective effects, as observed in both in vitro and in vivo experimental models. Mitochondrial dysfunction induced by reactive species plays a central role in the onset and progression of different human diseases. Thus, we have tested here whether a pretreatment (for 4 h) with EM (at 40 µM) would be able to promote mitochondrial protection in the human neuroblastoma SH-SY5Y cells exposed to the pro-oxidant agent hydrogen peroxide (H2O2). We found that the pretreatment with EM suppressed the effects of H2O2 on the activity of the mitochondrial complexes I and V, as well as on the production of adenosine triphosphate (ATP) and on the mitochondrial membrane potential (MMP). EM also prevented the H2O2-induced collapse in the tricarboxylic acid cycle (TCA) function. An anti-inflammatory role for EM was also observed in this experimental model, since this anthraquinone decreased the secretion of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) by the H2O2-challenged cells. Inhibition of the adenosine monophosphate-activated protein kinase (AMPK) or silencing of the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) abolished the protection induced by EM in the H2O2-treated cells. Therefore, EM prevented the H 2O2-induced mitochondrial dysfunction and pro-inflammatory state in the SH-SY5Y cells by an AMPK/Nrf2-dependent manner. Keywords Emodin · Mitochondria · Antioxidant · Anti-inflammatory · AMPK · Nrf2
Introduction Electronic supplementary material The online version of this article (https://doi.org/10.1007/s11064-020-03181-1) contains supplementary material, which is available to authorized users. * Marcos Roberto de Oliveira [email protected]; [email protected] 1
Grupo de Estudos em Neuroquímica e Neurobiologia de Moléculas Bioativas, Universidade Federal de Mato Grosso (UFMT), Av. Fernando Corrêa da Costa, 2367, Cuiaba, MT CEP 78060‑900, Brazil
2
Programa de Pós‑Graduação em Bioquímica e Bioprospecção (PPGBBIO), Centro de Ciências Químicas, Farmacêuticas e de Alimentos (CCQFA), Instituto de Biologia, Universidade Federal de Pelotas (UFPel), Pelotas, RS, Brazil
3
Departamento de Ciências da Natureza, Campus Universitário de Rio das Ostras – Universidade Federal Fluminense (UFF), Rio de Janeiro, Brazil
The trihydroxyanthraquinone emodin (EM; 1,3,8-trihydroxy-6-methylanthracene-9,10-dione; C15H10O5) has been viewed as an antioxidant, anti-inflammatory, and anti-tumor agent in several experimental
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