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Fatigue is a common health issue in today's society worldwide. Finding anti-fatigue functional substances seems warranted to alleviate fatigue-related issues. The Lateolabrax japonicuspeptides (LPH) obtained viaenzymatic hydrolysis were identified being rich in Glu, Gly, and hydrophobic amino acids, which exhibited antioxidant properties. However, other biological functions of LPH have yet to be reported. This study main goal was to investigate the anti-fatigue effects of LPH viaa fatigue mice model, and further to elucidate its underlying mechanism using in vivoassay. The results indicated that LPH exhibited strong antioxidant activity and stability in vitro. Meanwhile, LPH significantly extended the swimming time of mice, while also decreasing fatigue marker levels (LA, BUN, CK, and MDA) in serum concurrently by increased levels of antioxidant enzymes, blood glucose, and Na+-K+-ATPase. Histopathological examination revealed that LPH effectively improved tissue damage caused by fatigue. Mechanistically, LPH upregulated the gene and protein expression of Nrf2 and AMPK, indicating its regulatory role in Keap1/Nrf2 and AMPK/SIRT1/PGC-1α/NRF1 signaling pathways. Furthermore, the study demonstrated that LPH could modulate the abundance and balance of fatigue-related gut microbiota (Butyricimonas, Helicobacter, Monoglobus, and Turicibacter). In summary, these findings indicated that LPH exerted its anti-fatigue effect by improving energy metabolism and reducing oxidative stress, suggesting its potential as a promising functional anti-fatigue nutraceutical in food industry.

A sustainable solution to the dramatic spread of antibiotic resistance threatening public health security is the development of antibiotic-free antimicrobial substances. Inspired by natural host defense mechanisms involving amino-terminal copper−nickel binding motif (ATCUN) antimicrobial peptides (AMPs), we have designed and prepared an artificial complex (Cu@G-AMPs) incorporating single-atom Cu catalysts for antibacterial therapy. The substrate of the complex, formed from guanine doped with abundant heteroatoms, anchored single Cu atoms with a coordination number of 2 and an average bond length of 1.91Å. Interestingly, Cu@G-AMPs, exhibiting Fenton-like catalytic activity, caused the inactivation of methicillin-resistant Staphylococcus aureus(MRSA) by generating and delivering reactive oxygen species (ROS) cargo. Mechanistically, the intrinsic stress response system of MRSA underwent an irreversible collapse when Cu@G-AMPs initiated its offensive program associated with non-specific targets. Furthermore, Cu@G-AMPs, which inherited the immunomodulatory properties of AMPs, sequentially carried out the functions of pulling edge closure, stabilizing granulation tissue, promoting collagen fiber proliferation, alleviating inflammation, and promoting neovascularization in wound areas infected by MRSA. Our results show that Cu@G-AMPs will provide a new perspective on untangling the complex regulatory networks that resistant bacteria have cultivated to deactivate commercial antibiotics.