Inhibitory effect of carvacrol on lipopolysaccharide-induced memory impairment in rats
10.4196/kjpp.2020.24.1.27
- Author:
Bombi LEE
1
;
Mijung YEOM
;
Insop SHIM
;
Hyejung LEE
;
Dae hyun HAHM
Author Information
1. Acupuncture and Meridian Science Research Center, College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea. bombi@khu.ac.kr
- Publication Type:Original Article
- Keywords:
Brain-derived neurotrophic factor;
Cytokines;
Inflammation;
Lipopolysaccharides;
Memory
- MeSH:
Animals;
Brain;
Brain-Derived Neurotrophic Factor;
Cyclooxygenase 2;
Cytokines;
Discrimination (Psychology);
Food Additives;
Hippocampus;
Inflammation;
Lateral Ventricles;
Lipopolysaccharides;
Memory;
Necrosis;
Neurodegenerative Diseases;
Neuroprotective Agents;
Phenol;
Prefrontal Cortex;
Rats;
RNA, Messenger;
Toll-Like Receptor 4
- From:The Korean Journal of Physiology and Pharmacology
2020;24(1):27-37
- CountryRepublic of Korea
- Language:English
-
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.
