Key Laboratory of Agricultural Microbiomics and Precision Application, Ministry of Agriculture and Rural Affairs, Guangdong Provincial Key Laboratory of Microbial Safety and Health, State Key Laboratory of Applied Microbiology Southern China, Institute of Microbiology, Guangdong Academy of Sciences, Guangzhou 510070, China.
Department of Food Science and Engineering, Institute of Food Safety and Nutrition, College of Science & Engineering, College of Life Science and Technology, Jinan University, Guangzhou 510632, China.
J Agric Food Chem. 2023 Aug 16;71(32):12203-12215. doi: 10.1021/acs.jafc.3c02918. Epub 2023 Aug 2.
Selenopeptides are promising candidates for intervening in neuroinflammation; however, the key role of selenium (Se) in selenopeptides remains poorly understood. To address this gap, we compared the neuroprotective effects of selenopeptide Val-Pro-Arg-Lys-Leu-SeMet (namely, Se-P1) and its native peptide Val-Pro-Arg-Lys-Leu-Met (namely, P1). Our results demonstrate that Se-P1 treatment exhibits superior antioxidant and antineuroinflammatory effects in PC12 cells and lipopolysaccharide (LPS)-injured mice compared to P1. Moreover, the administration of Se-P1 and P1 resulted in a shift in the gut microbiota composition. Notably, during LPS-induced injury, Se-P1 treatment demonstrated greater stability in maintaining gut microbiota composition compared to P1 treatment. Specifically, Se-P1 may have a positive impact on gut microbiota dysbiosis by modulating inflammatory-related bacteria such as enhancing abundance while reducing that of . Furthermore, the alteration of metabolites induced by Se-P1 treatment exhibited a significant correlation with gut microbiota, subsequently modulating the inflammatory-related metabolic pathways including histidine metabolism, lysine degradation, and purine metabolism. These findings suggest that organic Se contributes to the bioactivities of Se-P1 in mitigating neuroinflammation in LPS-injured mice compared to P1. These findings hold significant value for the development of potential preventive or therapeutic strategies against neurodegenerative diseases and introduce novel concepts in selenopeptide nutrition and supplementation recommendations.
硒肽是干预神经炎症的有前途的候选物；然而，硒在硒肽中的关键作用仍知之甚少。为了解决这一差距，我们比较了硒肽 Val-Pro-Arg-Lys-Leu-SeMet（即 Se-P1）及其天然肽 Val-Pro-Arg-Lys-Leu-Met（即 P1）的神经保护作用。我们的结果表明，与 P1 相比，Se-P1 处理在 PC12 细胞和脂多糖（LPS）损伤的小鼠中表现出更好的抗氧化和抗神经炎症作用。此外，Se-P1 和 P1 的给药导致肠道微生物组组成发生变化。值得注意的是，在 LPS 诱导的损伤期间，与 P1 处理相比，Se-P1 处理在维持肠道微生物组组成方面表现出更大的稳定性。具体而言，Se-P1 可能通过调节与炎症相关的细菌（如增强丰度和减少丰度）对肠道微生物失调产生积极影响。此外，与 Se-P1 处理相关的代谢物的改变与肠道微生物群显著相关，随后调节与炎症相关的代谢途径，包括组氨酸代谢、赖氨酸降解和嘌呤代谢。这些发现表明，与 P1 相比，有机硒有助于 LPS 损伤小鼠中 Se-P1 减轻神经炎症的生物活性。这些发现为开发针对神经退行性疾病的潜在预防或治疗策略提供了重要价值，并在硒肽营养和补充建议方面引入了新概念。
