pISSN 1226-4512 eISSN 2093-3827

Article

home Article View

Original Article

Korean J Physiol Pharmacol 2020; 24(1): 27-37

Published online January 1, 2020 https://doi.org/10.4196/kjpp.2020.24.1.27

Copyright © The Korean Journal of Physiology & Pharmacology.

Inhibitory effect of carvacrol on lipopolysaccharide-induced memory impairment in rats

Bombi Lee1,2,*, Mijung Yeom1, Insop Shim1,3, Hyejung Lee1, and Dae-hyun Hahm1,3

1Acupuncture and Meridian Science Research Center, College of Korean Medicine, Kyung Hee University, 2Center for Converging Humanities, Kyung Hee University, 3Department of Physiology, College of Medicine, Kyung Hee University, Seoul 02447, Korea

Correspondence to:*Bombi Lee
E-mail: bombi@khu.ac.kr

Received: June 12, 2019; Revised: October 17, 2019; Accepted: November 10, 2019

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.

Abstract

Neuroinflammation is an important process underlying a wide variety of neurodegenerative diseases. Carvacrol (CAR) is a phenolic monoterpene commonly used as a food additive due to its antibacterial properties, but it has also been shown to exhibit strong antioxidative, anti-inflammatory, and neuroprotective effects. Here, we sought to investigate the effects of CAR on inflammation in the hippocampus and prefrontal cortex, as well as the molecular mechanisms underlying these effects. In our study, lipopolysaccharide was injected into the lateral ventricle of rats to induce memory impairment and neuroinflammation. Daily administration of CAR (25, 50, and 100 mg/kg) for 21 days improved recognition, discrimination, and memory impairments relative to untreated controls. CAR administration significantly attenuated expression of several inflammatory factors in the brain, including interleukin-1β, tumor necrosis factor-α, and cyclooxygenase-2. In addition, CAR significantly increased expression of brain-derived neurotrophic factor (BDNF) mRNA, and decreased expression of Toll-like receptor 4 (TLR4) mRNA. Taken together, these results show that CAR can improve memory impairment caused by neuroinflammation. This cognitive enhancement is due to the anti-inflammatory effects of CAR medicated by its regulation of BDNF and TLR4. Thus, CAR has significant potential as an inhibitor of memory degeneration in neurodegenerative diseases.

Keywords: Brain-derived neurotrophic factor, Cytokines, Inflammation, Lipopolysaccharides, Memory