Chicoric acid (CA), a natural phenolic acid extracted from chicory and the echinacea (purple coneflower) plant ( Echinacea purpurea ), has been regarded as a nutraceutical that has powerful antioxidant and antiobesity activities. We investigated the inhibitory effects of CA on systemic inflammation‐induced neuroinflammation, amyloidogenesis, and cognitive impairment. C57BL/6J mice were treated with 0.05% CA in the drinking water for 45 d. The mice were then treated by intraperitoneal injection of lipopolysaccharide (LPS). It was found that CA prevented LPS‐induced memory impairment and neuronal loss through behavioral tests and histological exam‐ination. Furthermore, amyloidogenesis in the CNS was detected. The results showed that CA prevented LPS‐induced increases in amyloid β (1–42 specific) (Aβ _1–42 ) accumulation, levels of amyloid precursor protein, and neuronal β‐secretase 1 (BACE1), as well as the equilibrium cholinergic system in mouse brain. Moreover, CA down‐regulated LPS‐induced glial overactivation by inhibiting the MAPK and NF‐κB pathway. Consequently, CA reduced the levels of NF‐κB transcriptionally regulated inflammatory mediators and cytokines such as iNOS, cyclooxygenase‐2 (COX‐2), IL‐1β, and TNF‐α in both mouse brain and BV2 microglial cells. These results demonstrated that CA alleviated memory impairment and amyloidogenesis triggered by LPS through suppressing NF‐κB transcriptional pathway, suggesting that CA might be a plausible therapeutic intervention for neuroinflammation‐related diseases such as Alzheimer disease. —Liu, Q., Chen, Y., Shen, C., Xiao, Y., Wang, Y., Liu, Z., Liu, X. Chicoric acid supplementation prevents systemic inflammation‐induced memory impairment and amyloidogenesis via inhibition of NF‐κB. FASEB J . 31, 1494–1507 (2017) www.fasebj.org

The incidence of lipid metabolism disorder and obesity that is caused by high-calorie diets is increasing year by year, which has become an urgent global health problem. This study was performed to explore the intervention effects of polysaccharides that were extracted from Auricularia auricula-judae resources in the Qinba Mountain area on nutritional obesity in C57BL/6J mice that was induced by high fat and high fructose diets (HFFD) and to investigate their underlying molecular mechanisms. The results showed that dietary supplementation of Auricularia auricula-judae polysaccharides (AAP) significantly improved mice’s insulin resistance state, altered serum lipid metabolites, and slowed down body weight gain that was induced by HFFD. In addition, AAP supplementation decreased inflammatory factor levels and alleviated liver histomorphology changes. Furthermore, AAP down-regulated liver adipogenic-related gene expressions, suppressed cholesterol synthesis-related gene levels, up-regulated fatty acid β-oxidation-related gene expressions, and promoted cholesterol efflux-related gene expressions, thus improving mice hepatic lipid metabolism homeostasis. Moreover, the intervention effects were closely related to mitochondrial function. These results provide a scientific basis for the further development and utilization of Auricularia auricula-judae resources in the Qinba Mountain area.

Personalized diets change the internal metabolism of organisms, which, in turn, affects the health of the body; this study was performed to explore the regulatory effects of polysaccharides extracted from Auricularia auricula on the overall metabolism and gut microbiota in normal C57BL/6J mice. The study was conducted using metabolomic and microbiomic methods to provide a scientific basis for further development and use of Auricularia auricula resources in the Qinba Mountains and in nutritional food with Auricularia auricula polysaccharides (AAP) as the main functional component. Based on LC-MS/MS metabolomic results, 51 AAP-regulated metabolites were found, mainly enriched in the arginine biosynthesis pathway, which had the highest correlation, followed by the following metabolisms: arginine and proline; glycine, serine and threonine; and glycerophospholipid, along with the sphingolipid metabolism pathway. Furthermore, supplementation of AAP significantly changed the composition of the mice intestinal flora. The relative abundance levels of Lactobacillus johnsonii, Weissella cibaria, Kosakonia cowanii, Enterococcus faecalis, Bifidobacterium animalis and Bacteroides uniformis were markedly up-regulated, while the relative abundance of Firmicutes bacterium M10-2 was down-regulated. The bioactivities of AAP may be related to the regulatory effects of endogenous metabolism and gut microbiota composition.

Chicoric acid promoted SH-SY5Y cells autophagy and inhibited cells apoptosis stimulated by microglia conditioned culture medium via inhibiting the release of microglia inflammatory factors and promoting mitochondrial function and energy metabolism.