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Original Article

Korean J Physiol Pharmacol 2022; 26(6): 415-425

Published online November 1, 2022

Copyright © Korean J Physiol Pharmacol.

Myricetin prevents sleep deprivation-induced cognitive impairment and neuroinflammation in rat brain via regulation of brain-derived neurotropic factor

Bongjun Sur1 and Bombi Lee1,2,*

1Acupuncture and Meridian Science Research Center, Kyung Hee University, 2Center for Converging Humanities, Kyung Hee University, Seoul 02447, Korea

Correspondence to:Bombi Lee

Author contributions: B.S. participated in animal experiments including behavioral tests, and performed most experiments, data analysis. B.L. wrote the draft of the paper, revised the manuscript, and directed the study, contributed to the discussion, edited and approved the manuscript. All authors read and approved the final manuscript.

Received: October 7, 2021; Revised: September 15, 2022; Accepted: September 15, 2022

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.


Memory formation in the hippocampus is formed and maintained by circadian clock genes during sleep. Sleep deprivation (SD) can lead to memory impairment and neuroinflammation, and there remains no effective pharmacological treatment for these effects. Myricetin (MYR) is a common natural flavonoid that has various pharmacological activities. In this study, we investigated the effects of MYR on memory impairment, neuroinflammation, and neurotrophic factors in sleep-deprived rats. We analyzed SD-induced cognitive and spatial memory, as well as pro-inflammatory cytokine levels during SD. SD model rats were intraperitoneally injected with 10 and 20 mg/kg/day MYR for 14 days. MYR administration significantly ameliorated SD-induced cognitive and spatial memory deficits; it also attenuated the SD-induced inflammatory response associated with nuclear factor kappa B activation in the hippocampus. In addition, MYR enhanced the mRNA expression of brain-derived neurotropic factor (BDNF) in the hippocampus. Our results showed that MYR improved memory impairment by means of anti-inflammatory activity and appropriate regulation of BDNF expression. Our findings suggest that MYR is a potential functional ingredient that protects cognitive function from SD.

Keywords: Brain-derived neurotrophic factor, Flavonoids, Inflammation, Memory, Sleep deprivation