Comparison of Neuroprotection and Regulating Properties on Gut Microbiota between Selenopeptide Val-Pro-Arg-Lys-Leu-SeMet and Its Native Peptide Val-Pro-Arg-Lys-Leu-Met In Vitro and In Vivo.

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 Lactobacillus abundance while reducing that of Lachnospiraceae_NK4A136_group. 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.

Moderate precipitation reduction enhances nitrogen cycling and soil nitrous oxide emissions in a semi-arid grassland.

The ongoing climate change is predicted to induce more weather extremes such as frequent drought and high-intensity precipitation events, causing more severe drying-rewetting cycles in soil. However, it remains largely unknown how these changes will affect soil nitrogen (N)-cycling microbes and the emissions of potent greenhouse gas nitrous oxide (N2 O). Utilizing a field precipitation manipulation in a semi-arid grassland on the Loess Plateau, we examined how precipitation reduction (ca. -30%) influenced soil N2 O and carbon dioxide (CO2 ) emissions in field, and in a complementary lab-incubation with simulated drying-rewetting cycles. Results obtained showed that precipitation reduction stimulated plant root turnover and N-cycling processes, enhancing soil N2 O and CO2 emissions in field, particularly after each rainfall event. Also, high-resolution isotopic analyses revealed that field soil N2 O emissions primarily originated from nitrification process. The incubation experiment further showed that in field soils under precipitation reduction, drying-rewetting stimulated N mineralization and ammonia-oxidizing bacteria in favor of genera Nitrosospira and Nitrosovibrio, increasing nitrification and N2 O emissions. These findings suggest that moderate precipitation reduction, accompanied with changes in drying-rewetting cycles under future precipitation scenarios, may enhance N cycling processes and soil N2 O emissions in semi-arid ecosystems, feeding positively back to the ongoing climate change.

Novel Selenium Peptides Obtained from Selenium-Enriched Cordyceps militaris Alleviate Neuroinflammation and Gut Microbiota Dysbacteriosis in LPS-Injured Mice.

Increasing attention focuses on the relationship between neuroinflammation and Alzheimer's disease (AD). The reports on the microbiota-gut-brain axis reveal that the regulation by gut microbiota is an effective way to intervene in neuroinflammation-related AD. In this study, two novel selenium peptides (Se-Ps), VPRKL(Se)M (Se-P1) and RYNA(Se)MNDYT (Se-P2), with neuroprotection effects were obtained from Se-enriched Cordyceps militaris. Se-P1 and Se-P2 pre-protection led to a 30 and 33% increase in the PC-12 cell viability compared to the damage group, respectively. Moreover, Se-Ps exhibited a significant pre-protection against LPS-induced inflammatory and oxidative stress in the colon and brain by inhibiting the production of pro-inflammatory mediators (p < 0.05) and malondialdehyde, as well as promoting anti-inflammatory cytokine level and antioxidant enzyme activity (p < 0.05), which may alleviate the cognitive impairment in LPS-injured mice (p < 0.05). Se-Ps not only repaired the intestinal mucosa damage of LPS-injured mice but also had a positive effect on gut microbiota dysbacteriosis by increasing the abundance of Lactobacillus and Alistipes and decreasing the abundance of Akkermansia and Bacteroides. Collectively, the antioxidant, anti-inflammatory, and regulating properties on gut microflora of Se-Ps contribute to their neuroprotection, supporting that Se-Ps could be a promising dietary supplement in the prevention and/or treatment of AD.