Eriodictyol alleviates lipopolysaccharide‐triggered oxidative stress and synaptic dysfunctions in BV‐2 microglial cells and mouse brain. Issue 9 (23rd April 2019)

• Record Type: Journal Article
• Authors: He, Pandi; Yan, Shikai; Wen, Xin; Zhang, Shuhan; Liu, Zhigang; Liu, Xuebo; Xiao, Chunxia
• Is Part Of: Journal of cellular biochemistry. Volume 120:Issue 9(2019)
• Page Start: 14756
• Page End: 14770
• Publication Date: 2019-04-23
• Subjects: eriodictyol -- lipopolysaccharide -- NF‐E2‐Related factor2/Kelch‐like ECH‐associated protein 1 -- oxidative stress -- synaptic dysfunctions; Cytochemistry -- Periodicals; 572
• DOI: 10.1002/jcb.28736
• Languages: English
• ISSNs: 0730-2312

Abstract

Abstract: 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. Abstract : Eriodictyol attenuates lipopolysaccharide‐induced oxidative stress, neuroinflammation, and synaptic dysfunctions partially through mitogen‐activated protein kinases, nuclear factor κB mediated by reactive oxygen species, silent information regulator 1, and NF‐E2‐Related factor2/Kelch‐like ECH‐associated protein 1 signal pathways in C57BL/6J male mice and BV‐2 microglial cells.