PMID- 22476923
OWN - NLM
STAT- MEDLINE
DCOM- 20120907
LR  - 20231213
IS  - 1573-7365 (Electronic)
IS  - 0885-7490 (Linking)
VI  - 27
IP  - 2
DP  - 2012 Jun
TI  - Chronic cigarette smoke exposure enhances brain-derived neurotrophic factor 
      expression in rats with traumatic brain injury.
PG  - 197-204
LID - 10.1007/s11011-012-9294-x [doi]
AB  - The involvement of brain-derived neurotrophic factor (BDNF) in regulating 
      neuronal survival during neuron differentiation, growth, and maturation, and 
      during the regeneration of injured nerve cells, has already been documented. In 
      experimental Parkinson's disease, chronic exposure to cigarette smoke increased 
      BDNF levels and survival of dopaminergic neurons. BDNF is also elevated in 
      traumatic brain injury (TBI), where it is potentially involved in post-injury 
      repair and regeneration. The aim of this study was to investigate the effects of 
      chronic exposure to cigarette smoke on BDNF expression and apoptosis in rats with 
      TBI. Three groups of rats were compared: rats with TBI after chronic exposure to 
      cigarette smoke, rats with TBI and no exposure to cigarette smoke, and 
      sham-operated rats. BDNF mRNA expression in the hippocampus increased from 2 to 
      24 h after TBI, and chronic exposure to cigarette smoke upregulated TBI-induced 
      BDNF mRNA elevation at 0, 2, 4, 12, and 24 h after head injury. The BDNF protein 
      levels generally corresponded to the mRNA levels in the hippocampal region. 
      Compared to the TBI group without smoke exposure, chronic cigarette smoke 
      exposure in rats inhibited the decrease of the Bcl-2/Bax ratio and reduced P53 
      expression and apoptosis 24 h after TBI. In addition, neuronal damage in the 
      parietal and cingulate cortex 7 days after TBI was less extensive in rats exposed 
      to cigarette smoke. In conclusion, although chronic exposure to cigarette smoke 
      is a risk factor for myocardial and pulmonary disease, cigarette smoke exposure 
      increases BDNF expression after TBI and thereby can play a neuroprotective role.
FAU - Lee, I-Neng
AU  - Lee IN
AD  - Department of Neurosurgery, Chang Gung Memorial Hospital, Pu Tz City, Chia-Yi, 
      Taiwan.
FAU - Lin, Martin Hsiu-Chu
AU  - Lin MH
FAU - Chung, Chiu-Yen
AU  - Chung CY
FAU - Lee, Ming-Hsueh
AU  - Lee MH
FAU - Weng, Hsu-Huei
AU  - Weng HH
FAU - Yang, Jen-Tsung
AU  - Yang JT
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120403
PL  - United States
TA  - Metab Brain Dis
JT  - Metabolic brain disease
JID - 8610370
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Coloring Agents)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 0 (RNA, Messenger)
RN  - 0 (Smoke)
RN  - 0 (Tumor Suppressor Protein p53)
RN  - 0 (bcl-2-Associated X Protein)
SB  - IM
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Brain Injuries/*metabolism
MH  - Brain-Derived Neurotrophic Factor/*biosynthesis
MH  - Chronic Disease
MH  - Coloring Agents
MH  - Hippocampus/drug effects/metabolism
MH  - Immunohistochemistry
MH  - In Situ Hybridization
MH  - Male
MH  - Proto-Oncogene Proteins c-bcl-2/biosynthesis
MH  - RNA, Messenger/biosynthesis/genetics
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Real-Time Polymerase Chain Reaction
MH  - Signal Transduction/drug effects
MH  - Smoke/*adverse effects
MH  - *Nicotiana
MH  - Tumor Suppressor Protein p53/biosynthesis
MH  - bcl-2-Associated X Protein/biosynthesis
EDAT- 2012/04/06 06:00
MHDA- 2012/09/08 06:00
CRDT- 2012/04/06 06:00
PHST- 2011/10/04 00:00 [received]
PHST- 2012/03/15 00:00 [accepted]
PHST- 2012/04/06 06:00 [entrez]
PHST- 2012/04/06 06:00 [pubmed]
PHST- 2012/09/08 06:00 [medline]
AID - 10.1007/s11011-012-9294-x [doi]
PST - ppublish
SO  - Metab Brain Dis. 2012 Jun;27(2):197-204. doi: 10.1007/s11011-012-9294-x. Epub 
      2012 Apr 3.