Eriodictyol, a natural flavonoid mainly distributed in citrus fruits and peanut, has been well-documented with possession of excellent anti-inflammatory, antioxidant, and anticancer bioactivities. This work focus on the protective effects of eriodictyol on LPS-induced neuroinflammation, amyloidogenesis, cognitive impairment, and the potential mechanisms involved. Behavioral tests and histological examinations showed that eriodictyol significantly prevented the memory and neuronal damage triggered by LPS. Consistently, eriodictyol (100 mg/kg) reduced the formation of Aβ by 28.37 ± 16.71 pg/mL compared to the LPS group. In addition, high dose eriodictyol (100 mg/kg) also equilibrated the cholinergic system via suppressing AChE activity (0.1996 ± 0.0831 U/mgprot) and elevating ChAT activity (41.81 ± 24.72 U/g) as well as ACh level (5.093 ± 3.531 μg/mgprot) compared to the LPS group. Western blot results indicated that compared to the LPS group, eriodictyol suppressed LPS-induced glial overactivation (84.29% ± 27.21%) and regulated inflammatory mediators and cytokines by inhibiting the NF-κB and MAPK pathways. These results indicated that eriodictyol alleviated amyloidogenesis and memory impairment triggered by LPS via inhibiting TLR4, MAPKs, and PI3K/Akt, and activating Sirt1 pathways and thus blocking downstream translocation of NF-κB, which offers a potential nutritional preventive strategy for neuroinflammation diseases such as Alzheimer's disease (AD).
Oxidative stress takes part in the development of the neurodegenerative disease. Eriodictyol, a flavonoid, commonly presents in citrus fruits, which was well‐known for its various bioactivities. The purpose of this study was to investigate the neuroprotective effects of eriodictyol on lipopolysaccharide (LPS)‐induced neuroinflammation, oxidative stress, synaptic dysfunctions, and the potential mechanisms involved. We found that eriodictyol explicitly restored LPS‐triggered the decrease of cell viability and the mitochondrial potential as well as inflammation responses via mitogen‐activated protein kinases (MAPKs) and nuclear factor κB (NF‐κB) pathways regulated by reactive oxygen species (ROS). Besides, eriodictyol alleviated LPS‐induced oxidative stress via NF‐E2‐Related factor2/Kelch‐like ECH‐associated protein 1 (Nrf2/Keap1) pathway in vivo and in vitro. Furthermore, eriodictyol reduced LPS‐elicited synaptic dysfunctions via increasing the expression of silent information regulator 1 (Sirt1). Overall, eriodictyol protects LPS‐triggered oxidative stress, neuroinflammation, and synaptic dysfunctions partially through MAPKs, NF‐κB mediated by ROS, Sirt1, and Nrf2/Keap1 signal pathways, which further supports that eriodictyol is a potentially nutritional preventive strategy for oxidative stress‐related neurodegenerative diseases.
It is widely believed that diet and the gut microbiota are strongly related to the occurrence and progression of inflammatory bowel disease (IBD), but the effects of the interaction between dietary patterns and the gut microbiota on IBD have not been well elucidated. In this paper, we aim to explore the complex relationship between dietary patterns, gut microbiota, and IBD. We first comprehensively summarize the dietary patterns associated with IBD and found that dietary patterns can modulate the occurrence and progression of IBD through various signaling pathways, including mammalian target of rapamycin (mTOR), mitogen-activated protein kinases (MAPKs), signal transducer and activator of transcription 3 (STAT3) and nuclear factor kappa B (NF-kappa B). Besides, the gut microbiota performs a vital role in the progression of IBD, which can affect the expression of IBD susceptibility genes, such as dual oxidase 2 (DUOX2) and apolipoprotein A1 (APOAI), the intestinal barrier (in particular, the expression of tight junction proteins), immune function (especially the homeostasis between effector and regulatory T cells) and the physiological metabolism, in particular, short chain fatty acids (SCFAs), bile acids (BAs) and tryptophan metabolisms. Finally, we review the current knowledge on the interaction between dietary patterns and the gut microbiota in IBD and found that dietary patterns modulate the onset and progression of IBD, which is partly attributed to the regulation of the gut microbiota (especially SCFAs-producing bacteria and Escherichia coli). Faecalibacteria as “microbiomarkers” of IBD could be used as a target for dietary interventions to alleviate IBD. A comprehensive understanding of the interplay between dietary intake, gut microbiota, and IBD, which will facilitate the development of personalized dietary strategies based on the regulation of the gut microbiota in IBD and to expedite the era of precision nutritional interventions for IBD.
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