Redox Role of Lactobacillus casei Shirota Against the Cellular Damage Induced by 2,2'-Azobis (2-Amidinopropane) Dihydrochloride-Induced Oxidative and Inflammatory Stress in Enterocytes-Like Epithelial Cells.
Redox Role of Lactobacillus casei Shirota Against the Cellular Damage Induced by 2,2'-Azobis (2-Amidinopropane) Dihydrochloride-Induced Oxidative and Inflammatory Stress in Enterocytes-Like Epithelial Cells.
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DOI：
10.3389/fimmu.2018.01131
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发表时间：
2018
影响因子：
7.3
通讯作者：
Serafini M
中科院分区：
文献类型：
--
作者：
Finamore A;Ambra R;Nobili F;Garaguso I;Raguzzini A;Serafini M
在西方社会，一天中的大部分时间都是在餐后状态中度过的，氧化和炎症应激条件的存在使餐后应激成为参与心血管危险因素发展的重要因素。关于益生菌的抗炎作用已经积累了大量的证据，但关于肠道微生物区系调节与炎症应激相关的氧化还原失衡的机制尚不清楚。在此，我们旨在研究干酪乳杆菌Shirota(LS)在体外培养的肠细胞模型中诱导抗氧化反应以对抗氧化和炎症应激的能力。我们的结果表明，LS对肠细胞的预处理可以防止膜屏障的破坏和细胞内ROS的积累，调节胃肠谷胱甘肽过氧化物酶(GPX2)抗氧化酶的表达，并减少p65的磷酸化，支持NFR2和核因子kappa B通路参与益生菌激活抗氧化细胞防御。这些结果首次表明LS在保护肠道细胞免受AAPH诱导的氧化和炎症应激中具有氧化还原机制。
In western societies where most of the day is spent in the postprandial state, the existence of oxidative and inflammatory stress conditions makes postprandial stress an important factor involved in the development of cardiovascular risk factors. A large body of evidence have been accumulated on the anti-inflammatory effects of probiotics, but no information is available on the mechanisms through which intestinal microbiota modulates redox unbalance associated with inflammatory stress. Here, we aimed to investigate the ability of Lactobacillus casei Shirota (LS) to induce an antioxidant response to counteract oxidative and inflammatory stress in an in vitro model of enterocytes. Our results show that pretreatment of enterocytes with LS prevents membrane barrier disruption and cellular reactive oxygen species (ROS) accumulation inside the cells, modulates the expression of the gastro-intestinal glutathione peroxidase (GPX2) antioxidant enzyme, and reduces p65 phosphorylation, supporting the involvement of the Nfr2 and nuclear factor kappa B pathways in the activation of antioxidant cellular defenses by probiotics. These results suggest, for the first time, a redox mechanism by LS in protecting intestinal cells from AAPH-induced oxidative and inflammatory stress.