Abstract
Increasing level of inflammation and oxidative stress could lead to memory impairment. The purpose of this study was to determine the neuroprotective effects of walnut peptides against memory deficits induced by lipopolysaccharide (LPS) in mice and further to explore the underlying anti-inflammatory mechanisms against LPS-elicited inflammation in BV-2 cells. Results showed that walnut protein hydrolysate (WPH) and its low-molecular-weight fraction (WPHL) could ameliorate the memory deficits induced by LPS via normalizing the inflammatory response and oxidative stress in brain, especially WPHL. Furthermore, 18 peptides with anti-inflammatory activities on LPS-activated BV-2 cells were identified from WPHL and it was found that Trp, Gly, and Leu residues in peptides might contribute to the anti-inflammation. Meanwhile, the strong anti-inflammatory effects of LPF, GVYY, and APTLW might be related to their hydrophobic and aromatic amino acid residues as well. LPF, GVYY, and APTLW could reduce the content of proinflammatory mediators and cytokines by downregulating related enzyme expressions and mRNA expressions. Additionally, ROS and mitochondria homeostasis might also contribute to their anti-inflammatory effects.
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