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Sesamol supplementation prevents systemic inflammation‐induced memory impairment and amyloidogenesis via inhibition of nuclear factor kappaB
Author(s) -
Liu Zhigang,
Chen Yuwei,
Qiao Qinglian,
Sun Yali,
Liu Qian,
Ren Bo,
Liu Xuebo
Publication year - 2017
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201600734
Subject(s) - sesamol , neuroinflammation , inflammation , pharmacology , morris water navigation task , chemistry , nf κb , tumor necrosis factor alpha , medicine , biochemistry , endocrinology , antioxidant , hippocampal formation
Scope The aim of the present study was to investigate the inhibitory effects of sesamol, a phenolic lignan from sesame, on the systemic inflammation‐induced neuroinflammation and amyloidogenesis as well as memory impairment. Methods and results C57BL/6J mice were treated with 0.05% sesamol (w/v) in the drinking water for 7 weeks, and then the mice were treated by intraperitoneal injection of LPS (0.25 mg/kg) for 9 days. Sesamol supplementation significantly improved (by 36.9%) LPS‐induced decreased spontaneous alteration in Y‐maze test, as well as significantly restored LPS‐elicited mice cognitive deficits through restoring performances such as escape distance in Morris water maze test. Moreover, sesamol prevented LPS‐induced increases in Aβ 1‐42 formation, levels of amyloid precursor protein, and neuronal β‐secretase 1 (BACE1) in the brain. Sesamol reduced LPS‐induced glial over‐activation by inhibiting MAPK and NFκB pathway as well as expressions of inflammatory mediators such as IL‐1β and TNFα. Furthermore, LPS‐induced transcriptional factor NFκB DNA binding activity was also inhibited by sesamol as examined by the electrophoretic mobility shift assay and molecular modeling. Conclusion These results indicated that sesamol mitigated LPS‐induced amyloidogenesis and memory impairment via inhibiting NFκB signal pathway, suggesting that the compound might be plausible therapeutic intervention for neuroinflammation‐related diseases such as AD.