Dendropanax morbifera Léveille extract ameliorates D-galactose-induced memory deficits by decreasing inflammatory responses in the hippocampus.
10.5625/lar.2017.33.4.283
- Author:
Kwon Young LEE
1
;
Hyo Young JUNG
;
Dae Young YOO
;
Woosuk KIM
;
Jong Whi KIM
;
Hyun Jung KWON
;
Dae Won KIM
;
Yeo Sung YOON
;
In Koo HWANG
;
Jung Hoon CHOI
Author Information
1. Department of Anatomy, College of Veterinary Medicine and Institute of Veterinary Science, Kangwon National University, Chuncheon 24341, South Korea. jhchoi@kangwon.ac.kr
- Publication Type:Original Article
- Keywords:
Dendropanax morbifera extract;
D-galactose;
hippocampus;
inflammation;
memory
- MeSH:
Aging;
Animals;
Cytokines;
Galactose;
Hippocampus*;
Inflammation;
Interleukin-10;
Interleukin-4;
Interleukin-6;
Memory Disorders*;
Memory*;
Mice;
Microglia;
Swimming;
Tumor Necrosis Factor-alpha;
United Nations
- From:Laboratory Animal Research
2017;33(4):283-290
- CountryRepublic of Korea
- Language:English
-
Abstract:
In the present study, we examined the effects of Dendropanax morbifera Léveille leaf extract (DML) on D-galactose-induced morphological changes in microglia and cytokines, including pro-inflammatory cytokines (interleukin [IL]-1β, IL-6, and tumor necrosis factor [TNF]-α) and anti-inflammatory cytokines (IL-4 and IL-10) in the hippocampus. Administration of DML to D-galactose-treated mice significantly improved D-galactose-induced reduction in escape latency, swimming speed, and spatial preference for the target quadrant. In addition, administration of DML to D-galactose-treated mice significantly ameliorated the microglial activation and increases of IL-1β, IL-6, and TNF-α levels in the hippocampus. Administration of D-galactose significantly reduced IL-4 levels in the hippocampus, while administration of DML to D-galactose-treated mice significantly increased IL-4 level. However, we did not observe any significant changes in IL-10 levels in hippocampal homogenates. These results suggest that DML reduces D-galactose-induced mouse senescence by reducing pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α, as well as increasing anti-inflammatory cytokine IL-4.
