Ginsenoside Rg3 Alleviates Lipopolysaccharide-Induced Learning and Memory Impairments by Anti-Inflammatory Activity in Rats.
- Author:
Bombi LEE
1
;
Bongjun SUR
;
Jinhee PARK
;
Sung Hun KIM
;
Sunoh KWON
;
Mijung YEOM
;
Insop SHIM
;
Hyejung LEE
;
Dae Hyun HAHM
Author Information
1. Acupuncture and Meridian Science Research Center, College of Oriental Medicine, Kyung Hee University, Seoul 130-701, Korea. bombi@khu.ac.kr dhhahm@khu.ac.kr
- Publication Type:Original Article
- Keywords:
Lipopolysaccharide;
Memory;
Inflammation;
Ginsenoside Rg3;
Morris water maze;
Cyclooxygenase-2
- MeSH:
Alzheimer Disease;
Animals;
Brain;
Cyclooxygenase 2;
Hippocampus;
Immunohistochemistry;
Inflammation;
Interleukin-1beta;
Lateral Ventricles;
Learning*;
Memory*;
Models, Animal;
Nervous System Diseases;
Rats*;
Tumor Necrosis Factor-alpha;
Water
- From:Biomolecules & Therapeutics
2013;21(5):381-390
- CountryRepublic of Korea
- Language:English
-
Abstract:
The purpose of this study was to examine whether ginsenoside Rg3 (GRg3) could improve learning and memory impairments and inflammatory reactions induced by injecting lipopolysaccharide (LPS) into the brains of rats. The effects of GRg3 on proinflammatory mediators in the hippocampus and the underlying mechanisms of these effects were also investigated. Injection of LPS into the lateral ventricle caused chronic inflammation and produced deficits in learning in a memory-impairment animal model. Daily administration of GRg3 (10, 20, and 50 mg/kg, i.p.) for 21 consecutive days markedly improved the LPS-induced learning and memory disabilities demonstrated on the step-through passive avoidance test and Morris water maze test. GRg3 administration significantly decreased expression of pro-inflammatory mediators such as tumor necrosis factor-alpha, interleukin-1beta, and cyclooxygenase-2 in the hippocampus, as assessed by reverse transcription-polymerase chain reaction analysis and immunohistochemistry. Together, these findings suggest that GRg3 significantly attenuated LPS-induced cognitive impairment by inhibiting the expression of pro-inflammatory mediators in the rat brain. These results suggest that GRg3 may be effective for preventing or slowing the development of neurological disorders, including Alzheimer's disease, by improving cognitive and memory functions due to its anti-inflammatory activity in the brain.
