PMID- 30042685
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 1663-9812 (Print)
IS  - 1663-9812 (Electronic)
IS  - 1663-9812 (Linking)
VI  - 9
DP  - 2018
TI  - The Protective Effect of Astaxanthin on Cognitive Function via Inhibition of 
      Oxidative Stress and Inflammation in the Brains of Chronic T2DM Rats.
PG  - 748
LID - 10.3389/fphar.2018.00748 [doi]
LID - 748
AB  - Currently, there are no effective treatments for diabetes-related cognitive 
      dysfunction. Astaxanthin (AST), the most powerful antioxidant in nature, exhibits 
      diverse biological functions. In this study, we tried to explore whether AST 
      would ameliorate cognitive dysfunction in chronic type 2 diabetes mellitus (T2DM) 
      rats. The T2DM rat model was induced via intraperitoneal injection of 
      streptozotocin. Forty Wistar rats were divided into a normal control group, an 
      acute T2DM group, a chronic T2DM group, and an AST group (treated with AST at a 
      dose of 25 mg/kg three times a week). The Morris water maze test showed that the 
      percentage of time spent in the target quadrant of the AST group was identical to 
      that of the chronic T2DM group, while the escape latency of the AST group was 
      decreased in comparison to that of the chronic T2DM group. Histology of the 
      hippocampus revealed that AST ameliorated the impairment in the neurons of 
      diabetic rats. Western blot showed that AST could upregulate nuclear factor 
      erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) expression and 
      inhibit nuclear transcription factor kappa B (NF-kappaB) p65 activation in the 
      hippocampus. We found that AST increased the level of superoxide dismutase (SOD) 
      and decreased the level of malondialdehyde (MDA) in the hippocampus. In addition, 
      the levels of interleukin 1 beta (IL-1beta) and interleukin 6 (IL-6) were reduced in 
      the AST group compared with those in the chronic T2DM group. The findings of this 
      research imply that AST might inhibit oxidative stress and inflammatory responses 
      by activating the Nrf2-ARE signaling pathway.
FAU - Feng, Yonghao
AU  - Feng Y
AD  - Department of Endocrinology, Jinshan Hospital, Fudan University, Shanghai, China.
FAU - Chu, Aiqun
AU  - Chu A
AD  - Department of General Medicine, Shihua Community Health Service Center, Shanghai, 
      China.
FAU - Luo, Qiong
AU  - Luo Q
AD  - Department of Neurology, Huashan Hospital North, Fudan University, Shanghai, 
      China.
FAU - Wu, Men
AU  - Wu M
AD  - Department of Endocrinology, Jinshan Hospital, Fudan University, Shanghai, China.
FAU - Shi, Xiaohong
AU  - Shi X
AD  - Department of Endocrinology, Jinshan Hospital, Fudan University, Shanghai, China.
FAU - Chen, Yinghui
AU  - Chen Y
AD  - Department of Neurology, Huashan Hospital North, Fudan University, Shanghai, 
      China.
LA  - eng
PT  - Journal Article
DEP - 20180710
PL  - Switzerland
TA  - Front Pharmacol
JT  - Frontiers in pharmacology
JID - 101548923
PMC - PMC6048598
OTO - NOTNLM
OT  - Nrf2
OT  - astaxanthin
OT  - cytokines
OT  - inflammatory response
OT  - oxidative stress
OT  - type 2 diabetes mellitus
EDAT- 2018/07/26 06:00
MHDA- 2018/07/26 06:01
PMCR- 2018/07/10
CRDT- 2018/07/26 06:00
PHST- 2018/02/28 00:00 [received]
PHST- 2018/06/19 00:00 [accepted]
PHST- 2018/07/26 06:00 [entrez]
PHST- 2018/07/26 06:00 [pubmed]
PHST- 2018/07/26 06:01 [medline]
PHST- 2018/07/10 00:00 [pmc-release]
AID - 10.3389/fphar.2018.00748 [doi]
PST - epublish
SO  - Front Pharmacol. 2018 Jul 10;9:748. doi: 10.3389/fphar.2018.00748. eCollection 
      2018.