PMID- 28974442
OWN - NLM
STAT- MEDLINE
DCOM- 20180226
LR  - 20181202
IS  - 1873-6351 (Electronic)
IS  - 0278-6915 (Linking)
VI  - 109
IP  - Pt 1
DP  - 2017 Nov
TI  - Supplementation of lycopene attenuates oxidative stress induced neuroinflammation 
      and cognitive impairment via Nrf2/NF-kappaB transcriptional pathway.
PG  - 505-516
LID - S0278-6915(17)30569-0 [pii]
LID - 10.1016/j.fct.2017.09.050 [doi]
AB  - Oxidative stress, considered as a major culprit in brain aging, triggers 
      cognitive and memory impairment. Lycopene (LYC), a carotenoid pigment, possesses 
      potent antioxidative, anti-inflammatory, and neuroprotective properties. In the 
      present study, the effects of LYC on oxidative stress-induced cognitive defects 
      and the underlying mechanisms were determined. The behavioral tests, including 
      Y-maze test, locomotor activity and Morris water maze test, revealed that chronic 
      LYC supplementation (50 mg/kg bodyweight per day) alleviated d-galactose induced 
      CD-1 male mice cognitive impairments. LYC ameliorated histopathological damage 
      and restored brain derived neurotrophic factor (BDNF) levels in the hippocampus 
      of mice. LYC also significantly elevated antioxidant enzymes activities and 
      reduced levels of inflammatory cytokines in the d-galactose-treated mice serum. 
      Moreover, LYC treatment activated the mRNA expressions of antioxidant enzymes 
      HO-1 and NQO-1, and downregulated inflammatory cytokines IL-1beta and TNF-alpha in mice 
      hippocampus. Immunohistochemical results also demonstrated that LYC significantly 
      restored the expression of glial cells inflammatory makers Iba-1 and GFAP. 
      Furthermore, LYC attenuated neuronal oxidative damage through activation of Nrf2 
      signaling and inactivation of NF-kappaB translocation in a H(2)O(2)-induced SH-SY5Y 
      cell model. Therefore, these results illustrated that LYC could ameliorate 
      oxidative stress induced neuroinflammation and cognitive impairment possibly via 
      mediating Nrf2/NF-kappaB transcriptional pathway.
CI  - Copyright (c) 2017 Elsevier Ltd. All rights reserved.
FAU - Zhao, Beita
AU  - Zhao B
AD  - Laboratory of Functional Chemistry and Nutrition of Food, College of Food Science 
      and Engineering, Northwest A&F University, Yangling, China.
FAU - Ren, Bo
AU  - Ren B
AD  - Laboratory of Functional Chemistry and Nutrition of Food, College of Food Science 
      and Engineering, Northwest A&F University, Yangling, China.
FAU - Guo, Rui
AU  - Guo R
AD  - Laboratory of Functional Chemistry and Nutrition of Food, College of Food Science 
      and Engineering, Northwest A&F University, Yangling, China.
FAU - Zhang, Wentong
AU  - Zhang W
AD  - Laboratory of Functional Chemistry and Nutrition of Food, College of Food Science 
      and Engineering, Northwest A&F University, Yangling, China.
FAU - Ma, Shaobo
AU  - Ma S
AD  - Laboratory of Functional Chemistry and Nutrition of Food, College of Food Science 
      and Engineering, Northwest A&F University, Yangling, China.
FAU - Yao, Yuchen
AU  - Yao Y
AD  - Laboratory of Functional Chemistry and Nutrition of Food, College of Food Science 
      and Engineering, Northwest A&F University, Yangling, China.
FAU - Yuan, Tian
AU  - Yuan T
AD  - Laboratory of Functional Chemistry and Nutrition of Food, College of Food Science 
      and Engineering, Northwest A&F University, Yangling, China.
FAU - Liu, Zhigang
AU  - Liu Z
AD  - Laboratory of Functional Chemistry and Nutrition of Food, College of Food Science 
      and Engineering, Northwest A&F University, Yangling, China.
FAU - Liu, Xuebo
AU  - Liu X
AD  - Laboratory of Functional Chemistry and Nutrition of Food, College of Food Science 
      and Engineering, Northwest A&F University, Yangling, China. Electronic address: 
      xueboliu@aliyun.com.
LA  - eng
PT  - Journal Article
DEP - 20170930
PL  - England
TA  - Food Chem Toxicol
JT  - Food and chemical toxicology : an international journal published for the British 
      Industrial Biological Research Association
JID - 8207483
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Interleukin-1beta)
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (NF-kappa B)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 36-88-4 (Carotenoids)
RN  - SB0N2N0WV6 (Lycopene)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/genetics/metabolism
MH  - Carotenoids/*administration & dosage
MH  - Cognitive Dysfunction/*drug therapy/genetics/metabolism/psychology
MH  - Hippocampus/drug effects/metabolism
MH  - Humans
MH  - Interleukin-1beta/genetics/metabolism
MH  - Lycopene
MH  - Male
MH  - Maze Learning
MH  - Mice
MH  - NF-E2-Related Factor 2/genetics/*metabolism
MH  - NF-kappa B/genetics/*metabolism
MH  - Neurons/drug effects/metabolism
MH  - Neuroprotective Agents/*administration & dosage
MH  - Oxidative Stress/*drug effects
MH  - Tumor Necrosis Factor-alpha/genetics/metabolism
OTO - NOTNLM
OT  - Cognitive impairment
OT  - Lycopene
OT  - Neuroinflammation
OT  - Nrf2/NF-kappaB transcriptional pathway
OT  - Oxidative stress
EDAT- 2017/10/05 06:00
MHDA- 2018/02/27 06:00
CRDT- 2017/10/05 06:00
PHST- 2017/04/12 00:00 [received]
PHST- 2017/09/19 00:00 [revised]
PHST- 2017/09/29 00:00 [accepted]
PHST- 2017/10/05 06:00 [pubmed]
PHST- 2018/02/27 06:00 [medline]
PHST- 2017/10/05 06:00 [entrez]
AID - S0278-6915(17)30569-0 [pii]
AID - 10.1016/j.fct.2017.09.050 [doi]
PST - ppublish
SO  - Food Chem Toxicol. 2017 Nov;109(Pt 1):505-516. doi: 10.1016/j.fct.2017.09.050. 
      Epub 2017 Sep 30.