RESUMEN
In this study, an inulin-type fructan (PGPI-1-a) was isolated from the roots of Platycodon grandiflorum. PGPI-1-a was composed of (2 â 1)-linked ß-D-fructofuranose (Fruf) and a terminal α-d-glucopyranose (Glcp) with a molecular weight of 12.1 kDa. PM2.5 exposure has brought a great threat to human health in recent years. Therefore, this study explored the effect of PGPI-1-a on the intestinal microbial community structure of rats exposed to PM2.5 using the animal model of PM2.5 inhalation exposure. The results showed that PGPI-1-a could regulate the intestinal microbiota by partly restoring the perturbed levels of Peptoniphilaceae_[G-2] and Lachnospiraceae_[G-2] caused by PM2.5 exposure. In addition, the relative abundance of Butyrivibrio, a butyric acid-producing genera, significantly increased after PGPI-1-a intervention. These results indicated that PGPI-1-a could improve the imbalance of intestinal microbiota due to PM2.5 exposure to a certain extent.
Asunto(s)
Fructanos/farmacología , Microbioma Gastrointestinal/efectos de los fármacos , Inulina/farmacología , Material Particulado/efectos adversos , Platycodon/química , Animales , Butyrivibrio/efectos de los fármacos , Clostridiales/efectos de los fármacos , Fructanos/análisis , Humanos , Inulina/análisis , Masculino , Microbiota , Peso Molecular , Raíces de Plantas/química , RatasRESUMEN
The topic of gut microbiota is currently attracting considerable interest as a potential factor in Alzheimer's disease (AD). However, the extent and time course of alterations in the gut microbiota, and their effects on AD pathology remain uncertain. Herein, we compared the fecal microbiomes and fecal short chain fatty acid composition (SCFAs) between wild-type and AD model mice at different ages under strictly controlled specific pathogen free conditions, and also conducted microscopic investigations of intestinal structures. Our results showed that the microbiota composition and diversity were perturbed and the level of SCFAs was reduced in AD mice, predicting alterations in more than 30 metabolic pathways, which may be associated with amyloid deposition and ultrastructural abnormalities in AD mouse intestine. These findings indicate that AD pathology might not only affect brain function directly, but also exacerbate cognitive deficits through reducing the level of SCFAs via alterations of gut microbiota induced by intestinal amyloid deposition. Our data may support a role of gut microbiota, and suggest a novel route for therapeutic intervention in AD.