PMID- 28821706
OWN - NLM
STAT- MEDLINE
DCOM- 20180517
LR  - 20190606
IS  - 1643-3750 (Electronic)
IS  - 1234-1010 (Print)
IS  - 1234-1010 (Linking)
VI  - 23
DP  - 2017 Aug 19
TI  - Apigenin Ameliorates Post-Stroke Cognitive Deficits in Rats Through Histone 
      Acetylation-Mediated Neurochemical Alterations.
PG  - 4004-4013
AB  - BACKGROUND To identify the effect of apigenin on cognitive deficits of rats after 
      cerebral ischemia and reperfusion injury, and to investigate the potential 
      molecular mechanisms. MATERIAL AND METHODS The rats were given sodium butyrate 
      (NaB) or apigenin (20 or 40 mg/kg) for 28 days. Cognition was investigated by the 
      Morris water maze (MWM) test. On day 28, the rats were euthanized and their 
      hippocampal brain regions were used to identify biochemical and neurochemical 
      alterations. The content of histone deacetylase (HDAC) was measured by 
      enzyme-linked immunosorbent assay (ELISA). Western blot analysis was performed to 
      determine the levels of BDNF, phosphorylated cAMP response element-binding 
      protein (pCREB), acetylated H3, and acetylated H4. The mRNA expressions of 
      brain-derived neurotrophic factor (BDNF) and synapsin-I (Syn-I) were examined by 
      polymerase chain reaction (PCR). RESULTS The rats with chronic administration of 
      apigenin (20 and 40 mg/kg) showed better performance in the MWM task than the 
      model rats; there was no significant difference between the apigenin-treated and 
      NaB-treated rats. At the higher apigenin dose of 40 mg/kg, the HDAC content was 
      decreased, the BDNF level was markedly increased, and acetylated H3 and 
      acetylated H4 expressions and Syn-I expressions in the hippocampus was 
      upregulated compared with the model group. Apigenin at 20 mg/kg did not show 
      reversal of the neurochemical alterations. CONCLUSIONS The improvement effect of 
      apigenin on cognitive impairments after cerebral ischemia and reperfusion injury 
      may involve multiple mechanisms, such as the inhibition of HDAC, induction of 
      BDNF and Syn-I expression, and regulation of histone acetylation.
FAU - Tu, Fengxia
AU  - Tu F
AD  - Department of Physical Medicine and Rehabilitation, The 2nd Affiliated Hospital 
      and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 
      China (mainland).
FAU - Pang, Qiongyi
AU  - Pang Q
AD  - Department of Physical Medicine and Rehabilitation, The 2nd Affiliated Hospital 
      and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 
      China (mainland).
FAU - Huang, Tingting
AU  - Huang T
AD  - Department of Physical Medicine and Rehabilitation, The 2nd Affiliated Hospital 
      and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 
      China (mainland).
FAU - Zhao, Yun
AU  - Zhao Y
AD  - Department of Physical Medicine and Rehabilitation, The 2nd Affiliated Hospital 
      and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 
      China (mainland).
FAU - Liu, Meixia
AU  - Liu M
AD  - Department of Physical Medicine and Rehabilitation, The 2nd Affiliated Hospital 
      and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 
      China (mainland).
FAU - Chen, Xiang
AU  - Chen X
AD  - Department of Physical Medicine and Rehabilitation, The 2nd Affiliated Hospital 
      and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 
      China (mainland).
LA  - eng
PT  - Journal Article
DEP - 20170819
PL  - United States
TA  - Med Sci Monit
JT  - Medical science monitor : international medical journal of experimental and 
      clinical research
JID - 9609063
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Cyclic AMP Response Element-Binding Protein)
RN  - 0 (Histones)
RN  - 107-92-6 (Butyric Acid)
RN  - 7V515PI7F6 (Apigenin)
RN  - EC 3.5.1.98 (Histone Deacetylases)
SB  - IM
MH  - Acetylation
MH  - Animals
MH  - Apigenin/*pharmacology
MH  - Brain Ischemia/drug therapy/metabolism/pathology
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Butyric Acid/pharmacology
MH  - Cognition Disorders/drug therapy
MH  - Cognitive Dysfunction/*drug therapy/etiology/metabolism
MH  - Cyclic AMP Response Element-Binding Protein/metabolism
MH  - Hippocampus/drug effects/metabolism
MH  - Histone Deacetylases/metabolism
MH  - Histones/metabolism
MH  - Male
MH  - Maze Learning/drug effects
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reperfusion Injury/*drug therapy/metabolism/psychology
MH  - Stroke/*drug therapy/metabolism/*psychology
PMC - PMC5572783
COIS- Conflict of interest The author confirms that this article content has no 
      conflict of interest.
EDAT- 2017/08/20 06:00
MHDA- 2018/05/18 06:00
PMCR- 2017/08/19
CRDT- 2017/08/20 06:00
PHST- 2017/08/20 06:00 [entrez]
PHST- 2017/08/20 06:00 [pubmed]
PHST- 2018/05/18 06:00 [medline]
PHST- 2017/08/19 00:00 [pmc-release]
AID - 902770 [pii]
AID - 10.12659/msm.902770 [doi]
PST - epublish
SO  - Med Sci Monit. 2017 Aug 19;23:4004-4013. doi: 10.12659/msm.902770.