RESUMO
Cardiovascular disease (CVD) represents a substantial global health challenge, with its impact on mortality and morbidity rates surpassing that of cancer. The present study was designed to explore the cardioprotective properties of anthocyanin (ACN), a compound derived from black barley, against oxidative stress-induced damage in myocardial cells and to uncover the molecular mechanisms at play. Utilizing both in vitro and in vivo experimental models, our findings indicate that ACN notably reduced cell damage caused by oxidative stress and effectively prevented apoptosis. High-throughput RNA sequencing analysis has shed light on the mechanism by which ACN achieves its antioxidative stress effects, implicating the PTEN-Akt signaling pathway. ACN was found to modulate PTEN expression levels, which in turn influences the Akt pathway, leading to a reduction in apoptotic processes. This novel insight lays the groundwork for the potential clinical utilization of ACN in the management of CVD. While this study has shed light on some of the functions of ACN, it is important to recognize that natural compounds often interact with multiple molecular targets and engage in intricate signaling cascades. Future research endeavors will concentrate on further elucidating the regulatory mechanisms by which ACN influences PTEN expression, with the goal of enhancing our comprehension and expanding the therapeutic potential of ACN in the treatment of cardiovascular conditions.
RESUMO
Dairy products are susceptible to modifications in protein oxidation during heat processing, which can lead to changes in protein function, subsequently affecting intestinal health. Despite being a unique nutritional source, yak milk has not been thoroughly examined for the effects of its oxidized proteins on intestinal microbiota and metabolism. Hence, this study employed different heat treatment methods (low-temperature pasteurization, high-temperature pasteurization, and high-temperature sterilization) to induce oxidation in yak milk proteins. The study then assessed the degree of oxidation in these proteins and utilized mice as research subjects. Using metagenomics and metabolomics methods, this study examined the structure of intestinal microbial communities and metabolic products in mice consuming oxidized yak milk. The results showed a decrease in carbonyl and total thiol contents of yak milk proteins after different heat treatments, indicating that heat treatment causes oxidation in yak milk proteins. Metagenomic analysis of mouse intestinal microbiota revealed significant changes in 66 genera. In the high-temperature sterilization group (H), key differential genera included Verrucomicrobiales, Verrucomicrobiae, Akkermansiaceae, and 28 others. The high-temperature pasteurization group (M) mainly consisted of Latilactobacillus, Bacillus, and Romboutsia. The low-temperature pasteurization group (L) primarily comprised of Faecalibacterium, Chaetomium, Paenibacillaceae, Eggerthella, Sordariales, and 33 others. Functionally, compared to the control group (C), the H group upregulated translation and energy metabolism functions, the L group the M group significantly upregulated metabolism of other amino acids, translation, and cell replication and repair functions. Based on metabolomic analysis, differential changes in mouse metabolites could affect multiple metabolic pathways in the body. The most significantly affected metabolic pathways were phenylalanine metabolism, vitamin B6 metabolism, steroid hormone biosynthesis, and pantothenate and CoA biosynthesis. The changes were similar to the functional pathway analysis of mouse metagenomics, affecting amino acid and energy metabolism in mice. In summary, moderate oxidation of yak milk proteins exhibits a positive effect on mouse intestinal microbiota and metabolism. In conclusion, yak milk has a positive effect on mouse intestinal microflora and metabolism, and this study provides a scientific basis for optimizing dairy processing technology and further developing and applying yak milk.
