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褪黑素治疗对 K562 红白血病细胞氧化还原适应细胞机制的影响。

Influence of Melatonin Treatment on Cellular Mechanisms of Redox Adaptation in K562 Erythroleukemic Cells.

机构信息

Department of Biology, Universidade Estadual Paulista (UNESP), São José do Rio Preto 15054-000, SP, Brazil.

Department of Genetics and Evolution, Universidade Federal de São Carlos (UFSCar), São Carlos 13565-905, SP, Brazil.

出版信息

Genes (Basel). 2022 Dec 11;13(12):2337. doi: 10.3390/genes13122337.

DOI:10.3390/genes13122337
PMID:36553603
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9778059/
Abstract

Melatonin (MEL) presents well-documented pleiotropic actions against oxidative stress (OS), acting indirectly through activation of transcription factors, e.g., FoxO3 and Nrf2. Thus, this study aimed to investigate the possible modulating effects of MEL on the redox signaling pathways PI3K/AKT/FoxO3 and Keap1/Nrf2/ARE in K562 erythroleukemic cells subjected to OS induction. For this, the viability, and transcript levels of genes involved in redox adaptation were evaluated in K562 cells in different periods of erythroid differentiation: under OS induction by hydrogen peroxide (100 µM HO); treated with 1 nM (C1) and 1 mM (C2) MEL; and associated or not with stress induction. We observed a restoration of physiological levels of Nrf2 in both MEL concentrations under OS. The C1 was related to enhanced expression of antioxidant and proteasome genes through the Nrf2-ARE pathway, while C2 to the induction of FOXO3 expression, suggesting an involvement with apoptotic pathway, according to BIM transcript levels. The effects of MEL administration in these cells showed a period and dose-dependent pattern against induced-OS, with direct and indirect actions through different pathways of cellular adaptation, reinforcing the importance of this indolamine in the regulation of cellular homeostasis, being a promising therapeutic alternative for diseases that present an exacerbated OS.

摘要

褪黑素（MEL）具有明确的抗氧化应激（OS）的多效作用，通过激活转录因子（如 FoxO3 和 Nrf2）间接发挥作用。因此，本研究旨在探讨 MEL 对 K562 红白血病细胞 OS 诱导后 PI3K/AKT/FoxO3 和 Keap1/Nrf2/ARE 氧化还原信号通路的可能调节作用。为此，在不同的红细胞分化时期，评估了 MEL 对 K562 细胞氧化还原适应相关基因的转录水平和细胞活力的影响：在过氧化氢（100 µM HO）诱导的 OS 下；用 1 nM（C1）和 1 mM（C2）MEL 处理；以及是否与应激诱导相关。我们观察到在 OS 下，两种浓度的 MEL 都能使 Nrf2 恢复到生理水平。C1 通过 Nrf2-ARE 途径增强抗氧化和蛋白酶体基因的表达，而 C2 则诱导 FOXO3 的表达，根据 BIM 转录水平，这表明与凋亡途径有关。MEL 对这些细胞的作用表现出对诱导 OS 的时间和剂量依赖性模式，通过不同的细胞适应途径发挥直接和间接作用，这加强了这种吲哚胺在调节细胞内稳态中的重要性，为表现出过度 OS 的疾病提供了一种有前途的治疗选择。

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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eac5/9778059/9ed693433a22/genes-13-02337-g008.jpg
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Knockout Mouse Models for Peroxiredoxins.过氧化物还原酶基因敲除小鼠模型
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