Evaluation of the protective bioactivity and molecular mechanism verification of lactoferrin in an Alzheimer's mouse model with ulcerative enteritis

Abstract

The development of new drug therapies for Alzheimer's disease (AD) is an important research topic today, but the pathogenesis of AD has not been thoroughly studied, and there are still several shortcomings in existing drug therapies. Therefore, this study aimed to explore the molecular mechanism of lactoferrin (LF) in the treatments of AD and ulcerative colitis (UC) that is susceptible to AD, starting from the principle of one drug, two diseases, and the same treatment. This study used pathological staining and specific indicator staining to preliminarily evaluate the interventions of LF on UC injury and AD progression. We also used 16s RNA full-length sequencing to investigate the effect of LF on the abundance of intestinal microbiota in AD mice. Intestinal tissue and brain tissue metabolomics analysis were then used to screen specific metabolic pathways and preliminarily verify the metabolic mechanism of LF in alleviating the 2 diseases by regulating certain specific metabolites. Moreover, LF significantly changed the types and abundance of gut microbiota in AD mice complicated by UC. To conclude, this study proved the clinical phenomenon of AD susceptibility to UC, and verified the therapeutic effect of LF on 2 diseases. More importantly, we revealed the possible molecular mechanism of LF: Not only does it enrich the cognitive level of LF in alleviating AD by regulating the gut microbiota through the brain gut axis from the perspective of the theory of food nutrition promoting human health, but it also provides a practical basis for the subsequent research and development of LF and drug validation from the perspective of drug food homology.