期刊
JOURNAL OF CELLULAR BIOCHEMISTRY
卷 120, 期 9, 页码 14756-14770出版社
WILEY
DOI: 10.1002/jcb.28736
关键词
eriodictyol; lipopolysaccharide; NF-E2-Related factor2; Kelch-like ECH-associated protein 1; oxidative stress; synaptic dysfunctions
资金
- Natural Science Basic Research Plan in Shaanxi Province of China [2015JQ2039]
- Fundamental Research Funds for the Central Universities [2452016083]
- National Key Research and Development Program of China [2016YFD0400601]
- China Postdoctoral Science Foundation [2015M572603]
- National Natural Science Foundation of China [21403169]
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 kappa B (NF-kappa B) 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-kappa B 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.
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