PMID- 28100329
OWN - NLM
STAT- MEDLINE
DCOM- 20170726
LR  - 20200808
IS  - 1008-8830 (Print)
IS  - 1008-8830 (Linking)
VI  - 19
IP  - 1
DP  - 2017 Jan
TI  - [Protective effect of histone acetylation against cortical injury in neonatal 
      rats].
PG  - 81-87
AB  - OBJECTIVE: To investigate the protective effect of histone acetylation against 
      hypoxic-ischemic cortical injury in neonatal rats. METHODS: A total of 90 
      neonatal rats aged 3 days were divided into three groups: sham-operation, 
      cortical injury model, and sodium butyrate (a histone deacetylase inhibitor) 
      treatment. The rats in the model and the sodium butyrate treatment groups were 
      intraperitoneally injected with lipopolysaccharide (0.05 mg/kg), and then right 
      common carotid artery ligation was performed 2 hours later and the rats were put 
      in a hypoxic chamber (oxygen concentration 6.5%) for 90 minutes. The rats in the 
      sham-operation group were intraperitoneally injected with normal saline and the 
      right common carotid artery was only separated and exposed without ligation or 
      hypoxic treatment. The rats in the sodium butyrate treatment group were 
      intraperitoneally injected with sodium butyrate (300 mg/kg) immediately after 
      establishment of the cortical injury model once a day for 7 days. Those in the 
      sham-operation and the model groups were injected with the same volume of normal 
      saline. At 7 days after establishment of the model, Western blot was used to 
      measure the protein expression of histone H3 (HH3), acetylated histone H3 (AH3), 
      B-cell lymphoma/leukemia-2 (Bcl-2), Bcl-2-associated X protein (BAX), cleaved 
      caspase-3 (CC3), and brain-derived neurotrophic factor (BDNF). Immunofluorescence 
      assay was used to measure the expression of 5-bromo-2'-deoxyuridine (BrdU) as the 
      cortex cell proliferation index. RESULTS: The sodium butyrate treatment group had 
      a significantly lower HH3/AH3 ratio than the model group (P<0.05), which 
      suggested that the sodium butyrate treatment group had increased acetylation of 
      HH3. Compared with the model group, the sodium butyrate treatment group had a 
      significant increase in Bcl-2/Bax ratio, a significant reduction in CC3 
      expression, and a significant increase in BDNF expression (P<0.05). The sodium 
      butyrate treatment group had a significant increase in the number of 
      BrdU-positive cells in the cortex compared with the model group (P<0.05), and 
      BrdU was mainly expressed in the neurons. CONCLUSIONS: Increased histone 
      acetylation may protect neonatal rats against cortical injury by reducing 
      apoptosis and promoting regeneration of neurons. The mechanism may be associated 
      with increased expression of BDNF.
FAU - Huang, Ji-Chong
AU  - Huang JC
AD  - Department of Pediatrics, West China Second University Hospital, Sichuan 
      University, Chengdu 610041, China. mudz@scu.edu.cn.
FAU - Li, Ya-Fei
AU  - Li YF
FAU - Zhao, Feng-Yan
AU  - Zhao FY
FAU - Qu, Yi
AU  - Qu Y
FAU - Mu, De-Zhi
AU  - Mu DZ
LA  - chi
PT  - Journal Article
PL  - China
TA  - Zhongguo Dang Dai Er Ke Za Zhi
JT  - Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
JID - 100909956
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Histones)
RN  - 107-92-6 (Butyric Acid)
SB  - IM
MH  - Acetylation
MH  - Animals
MH  - Animals, Newborn
MH  - Apoptosis/drug effects
MH  - Brain-Derived Neurotrophic Factor/analysis
MH  - Butyric Acid/therapeutic use
MH  - Cerebral Cortex/*pathology
MH  - Female
MH  - Histones/*metabolism
MH  - Male
MH  - Rats
MH  - Rats, Sprague-Dawley
PMC - PMC7390123
EDAT- 2017/01/20 06:00
MHDA- 2017/07/27 06:00
PMCR- 2017/01/25
CRDT- 2017/01/20 06:00
PHST- 2017/01/20 06:00 [entrez]
PHST- 2017/01/20 06:00 [pubmed]
PHST- 2017/07/27 06:00 [medline]
PHST- 2017/01/25 00:00 [pmc-release]
AID - 10.7499/j.issn.1008-8830.2017.01.014 [pii]
AID - zgddekzz-19-1-81 [pii]
AID - 10.7499/j.issn.1008-8830.2017.01.014 [doi]
PST - ppublish
SO  - Zhongguo Dang Dai Er Ke Za Zhi. 2017 Jan;19(1):81-87. doi: 
      10.7499/j.issn.1008-8830.2017.01.014.