PMID- 23110519
OWN - NLM
STAT- MEDLINE
DCOM- 20131031
LR  - 20130214
IS  - 1563-5279 (Electronic)
IS  - 0020-7454 (Linking)
VI  - 123
IP  - 3
DP  - 2013 Mar
TI  - Changes of inflammatory cytokines and neurotrophins emphasized their roles in 
      hypoxic-ischemic brain damage.
PG  - 191-5
LID - 10.3109/00207454.2012.744755 [doi]
AB  - Inflammatory cytokines and neurotrophins play crucial roles in hypoxic-ischemic 
      brain damage (HIBD), but the expression changes of these proteins had not been 
      systematically studied. In this article, we compared the levels of tumor necrosis 
      factor alpha (TNF-alpha), intercellular adhesion molecule-1 (ICAM-1), interleukin 
      1beta (IL-1beta), nerve growth factor (NGF), and brain-derived neurotrophic factor 
      (BDNF) in the progression of HIBD and analyzed their correlations with apoptosis. 
      Seven-day-old pups of Sprague Dawley rats (n = 120) were randomly divided into 
      two groups: the sham-operated (control) group and the hypoxia-ischemia (HI) 
      group. To establish the hypoxic-ischemic encephalopathy model, the pups from the 
      HI group were subjected to left common carotid artery ligation followed by 
      exposure to 8% O2 and 92% N2 for 2.5 hr. Pups from both the groups were 
      sacrificed at 6, 24, 48, 72 hr and 7 days after hypoxia. The levels of TNF-alpha, 
      ICAM-1, IL-1beta, NGF, and BDNF in the brain tissues were measured by enzyme-linked 
      immunosorbent assay. The neuronal apoptosis was examined by flow cytometry. We 
      found that the levels of TNF-alpha, ICAM-1, IL-1beta, NGF, BDNF, and neuronal apoptosis 
      rate in neonatal rats with HIBD significantly increased at 6, 24, 48, and 72 hr 
      after hypoxia compared to the control group (p < .05) and returned back to normal 
      by 7 days. Furthermore, neuronal apoptosis rate was positively correlated with 
      the levels of TNF-alpha, ICAM-1, and IL-1beta and negatively correlated with the levels 
      of NGF and BDNF. In neonatal rats with HIBD, the brain reaches its peak levels of 
      damage by 24-72 hr after the injury. Inflammatory cytokines such as TNF-alpha, 
      ICAM-1, and IL-1beta contribute to neuronal apoptosis induced by HIBD, whereas 
      neurotrophins NGF and BDNF antagonize it.
FAU - Wang, Yun
AU  - Wang Y
AD  - The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan 
      Province, China. yunwangcn@163.com
FAU - Cao, Meng
AU  - Cao M
FAU - Liu, Aiqin
AU  - Liu A
FAU - Di, Wenyu
AU  - Di W
FAU - Zhao, Fen
AU  - Zhao F
FAU - Tian, Yunjiao
AU  - Tian Y
FAU - Jia, Jianwei
AU  - Jia J
LA  - eng
PT  - Journal Article
DEP - 20121207
PL  - England
TA  - Int J Neurosci
JT  - The International journal of neuroscience
JID - 0270707
RN  - 0 (Cytokines)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Nerve Growth Factors)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Cytokines/*physiology
MH  - Hypoxia, Brain/*metabolism/*pathology
MH  - Hypoxia-Ischemia, Brain/*metabolism/*pathology
MH  - Inflammation Mediators/*physiology
MH  - Nerve Growth Factors/*physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
EDAT- 2012/11/01 06:00
MHDA- 2013/11/01 06:00
CRDT- 2012/11/01 06:00
PHST- 2012/11/01 06:00 [entrez]
PHST- 2012/11/01 06:00 [pubmed]
PHST- 2013/11/01 06:00 [medline]
AID - 10.3109/00207454.2012.744755 [doi]
PST - ppublish
SO  - Int J Neurosci. 2013 Mar;123(3):191-5. doi: 10.3109/00207454.2012.744755. Epub 
      2012 Dec 7.