Selenomethionine and Allicin Synergistically Mitigate Intestinal Oxidative Injury by Activating the Nrf2 Pathway.

IF 3.9 3区 环境科学与生态学 Q2 ENVIRONMENTAL SCIENCES Toxics Pub Date : 2024-09-30 DOI:10.3390/toxics12100719
Yongshi Liu, Xi Lv, Heling Yuan, Xiaoming Wang, Jinhu Huang, Liping Wang
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Abstract

Oxidative stress frequently contributes to intestinal barrier injury in animals and humans. It was reported that both Selenomethionine (SeMet) and allicin exhibit protective effects against a range of diseases caused by oxidative stress. This study aimed to investigate the synergistic antioxidant effects and underlying mechanisms of SeMet and allicin on a H2O2-induced intestinal barrier injury model using IPEC-J2 cells and mice. The results showed that H2O2 induced severe oxidative stress, including a decrease in cell viability, antioxidant level, migration capacity, and cell integrity. SeMet and allicin exhibited significant synergistic anti-oxidative effects on intestinal epithelial cells. The combined use of SeMet and allicin increased SOD activity, GSH content, and GSH/GSSG ratio while decreasing MDA, NO, and ROS content levels. Furthermore, we found that SeMet and allicin synergistically activated the nuclear factor erythroid-related factor 2 (Nrf2)-NAD(P)H dehydrogenase [quinone] 1 (NQO1) signaling pathway and down-regulated endoplasmic reticulum stress (ER stress)-related proteins. However, the synergistic antioxidative and intestinal barrier protective effects of SeMet and allicin were abolished by Nrf2 inhibitor ML385 in vitro and in vivo. In conclusion, SeMet and allicin synergistically attenuate intestinal barrier injury induced by excessively oxidative stress through the activation of the Nrf2 signaling pathway and inhibition ER stress. These findings support that the combined use of SeMet and allicin could enhance antioxidative properties and alleviate intestinal injury in further clinical practice.

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硒蛋氨酸和大蒜素通过激活 Nrf2 通路协同缓解肠道氧化损伤
氧化应激经常导致动物和人类肠道屏障损伤。据报道,硒蛋氨酸(SeMet)和大蒜素对氧化应激引起的一系列疾病都有保护作用。本研究旨在利用 IPEC-J2 细胞和小鼠研究 SeMet 和大蒜素对 H2O2 诱导的肠屏障损伤模型的协同抗氧化作用及其内在机制。结果表明,H2O2 诱导了严重的氧化应激,包括细胞活力、抗氧化水平、迁移能力和细胞完整性的下降。SeMet 和大蒜素对肠上皮细胞具有显著的协同抗氧化作用。联合使用 SeMet 和大蒜素可提高 SOD 活性、GSH 含量和 GSH/GSSG 比率,同时降低 MDA、NO 和 ROS 含量水平。此外,我们还发现 SeMet 和大蒜素能协同激活核因子红细胞相关因子 2(Nrf2)-NAD(P)H 脱氢酶[醌]1(NQO1)信号通路,并下调内质网应激(ER 应激)相关蛋白。然而,SeMet 和大蒜素的协同抗氧化和肠屏障保护作用在体外和体内均被 Nrf2 抑制剂 ML385 削弱。总之,SeMet 和大蒜素通过激活 Nrf2 信号通路和抑制 ER 应激,协同减轻过度氧化应激引起的肠屏障损伤。这些研究结果支持在临床实践中联合使用 SeMet 和大蒜素可增强抗氧化性并减轻肠道损伤。
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来源期刊
Toxics
Toxics Chemical Engineering-Chemical Health and Safety
CiteScore
4.50
自引率
10.90%
发文量
681
审稿时长
6 weeks
期刊介绍: The Journal accepts papers describing work that furthers our understanding of the exposure, effects, and risks of chemicals and materials in humans and the natural environment as well as approaches to assess and/or manage the toxicological and ecotoxicological risks of chemicals and materials. The journal covers a wide range of toxic substances, including metals, pesticides, pharmaceuticals, biocides, nanomaterials, and polymers such as micro- and mesoplastics. Toxics accepts papers covering: The occurrence, transport, and fate of chemicals and materials in different systems (e.g., food, air, water, soil); Exposure of humans and the environment to toxic chemicals and materials as well as modelling and experimental approaches for characterizing the exposure in, e.g., water, air, soil, food, and consumer products; Uptake, metabolism, and effects of chemicals and materials in a wide range of systems including in-vitro toxicological assays, aquatic and terrestrial organisms and ecosystems, model mammalian systems, and humans; Approaches to assess the risks of chemicals and materials to humans and the environment; Methodologies to eliminate or reduce the exposure of humans and the environment to toxic chemicals and materials.
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