The human body is almost always facing the oxidative stress caused by foodborne aldehydes such as glyoxal (GO) and methylglyoxal (MGO), 4-hydroxyhexenal (HHE), and 4-hydroxynonenal (HNE). When these aldehydes build up, they can cause a range of harm. However, a probiotic, Clostridium butyricum, can increase nuclear factor erythroid-2 related factor 2 (Nrf2) and may have the potential to relieve oxidative stress. If C. butyricum is indeed resistant to aldehydes, the advantages (accessibility, convenience, and safety) will be of great significance compared with drugs. Unfortunately, whether C. butyricum can play a role in alleviating toxic effects of foodborne aldehydes in the intestine (the first line of defense against food-derived toxin) was unclear. To investigate these, we measured the viability, ROS, autophagy, and inflammatory cytokine expression of Caco-2 which were co-cultured with C. butyricum and stimulated by the four aldehydes via Nrf2 pathway (Staphylococcus aureus and Enterococcus faecium as controls). Then, we explored the link among C. butyricum, NLRP6, and Nrf2 signaling pathways when facing the stimuli. In the present study, we demonstrated that Clostridium butyricum relieved the oxidative stress induced by the aldehydes in Caco-2. Most interestingly, we found a "complementary" relationship between NLRP6 and Nrf2 in C. butyricum treatment under aldehyde stress. Our research not only makes a contribution to the popularization of C. butyricum as a probiotic-rich food instead of medicines but also sheds new light on the application of subsequent microecological formulation of C. butyricum. KEY POINTS: • The adverse effects are caused in a dose-dependent manner by foodborne aldehydes. • Clostridium butyricum can significantly ameliorate oxidative stress. • There is a "complementary" relationship between the NLRP6 and Nrf2 signaling pathways. • Using Clostridium butyricum foods to alleviate oxidative stress shows great prospects.

中文翻译：

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酪酸梭状芽胞杆菌对食品加工和脂质衍生的醛在Caco-2细胞中诱导的氧化应激的保护作用。

人体几乎总是面临由食源性醛（例如乙二醛（GO）和甲基乙二醛（MGO），4-羟基己烯醛（HHE）和4-羟基壬烯醛（HNE））引起的氧化应激。当这些醛积累时，会造成一系列危害。但是，益生菌丁酸梭菌可以增加核因子erythroid-2相关因子2（Nrf2），并且可能具有缓解氧化应激的潜力。如果酪酸梭菌确实对醛具有抗性，那么与药物相比，其优势（可及性，便利性和安全性）将具有重要意义。不幸的是，尚不清楚酪酸梭菌是否可以在减轻肠道中食源性醛的毒性作用中发挥作用（抵抗食物衍生毒素的第一道防线）。为了研究这些问题，我们测量了活力，ROS，自噬，与丁酸梭状芽孢杆菌共培养并通过Nrf2途径（金黄色葡萄球菌和粪肠球菌为对照）被四个醛刺激的Caco-2的炎性细胞因子表达。然后，我们探讨了丁酸梭菌，NLRP6和Nrf2信号通路在面对刺激时的联系。在本研究中，我们证明了丁酸梭菌可以缓解Caco-2中的醛类诱导的氧化应激。最有趣的是，我们发现在醛胁迫下丁酸梭菌处理中，NLRP6和Nrf2之间存在“互补”关系。我们的研究不仅为丁酸梭菌作为富含益生菌的食品而不是药物的普及做出了贡献，而且为随后的丁酸梭菌微生态制剂的应用提供了新的思路。关键点：•不良反应是由食源性醛以剂量依赖性方式引起的。•丁酸梭菌可以显着改善氧化应激。•NLRP6和Nrf2信号通路之间存在“互补”关系。•使用酪酸梭菌食品减轻氧化应激显示出广阔的前景。