PMID- 26554621
OWN - NLM
STAT- MEDLINE
DCOM- 20170404
LR  - 20170404
IS  - 1532-4281 (Electronic)
IS  - 1079-9893 (Linking)
VI  - 36
IP  - 4
DP  - 2016 Aug
TI  - Delayed neuroprotection against cerebral ischemia reperfusion injury: putative 
      role of BDNF and GSK-3beta.
PG  - 402-10
LID - 10.3109/10799893.2015.1108338 [doi]
AB  - AIM: Numerous studies have demonstrated the possible neuroprotective role of 
      lithium treatment against neurological disorders. However, the role of lithium in 
      delayed phase of neuronal death against focal ischemia has not been explored. 
      Therefore, the present study was designed to investigate the effect and molecular 
      mechanisms of post-lithium treatment against cerebral ischemic reperfusion (I/R) 
      injury and associated cognitive deficits in rats. METHODS: I/R injury was induced 
      by right middle cerebral artery occlusion and lithium (40 and 60 mg/kg) were 
      given intraperitoneally, 24 h after the insult and continued for 1 week with 24-h 
      interval. Using Lasser Doppler, cerebral blood flow was monitored before, during 
      and after MCAO induction. Besides behavioral, biochemical, and histological 
      evaluation, levels of tumor necrosis factor alpha (TNF-alpha) and brain-derived 
      neurotrophic factor (BDNF) were also estimated. RESULTS: I/R injury resulted in 
      significant elevation of neurological deficits, oxidative stress, 
      neuroinflammation, and cognitive impairments. We found that lithium injection, 
      24 h after I/R-injury continued for 1 week, dose dependently prevented behavioral 
      abnormality and cognitive impairments. Moreover, lithium attenuated the levels of 
      oxidative stress and pro-inflammatory-cytokines TNF-alpha level. Further, lithium 
      treatments significantly reduced neuronal damage and augmented healthy neuronal 
      count and improved neuronal density in hippocampus. These neuroprotective effects 
      of delayed lithium treatment were associated with upregulation of neurotrophic 
      factor BDNF levels. CONCLUSION: Delayed lithium treatment provides 
      neuroprotection against cerebral I/R injury and associated cognitive deficits by 
      upregulating BDNF expression that opens a new avenue to treat I/R injury even 
      after active cell death.
FAU - Taliyan, Rajeev
AU  - Taliyan R
AD  - a Department of Pharmacy , Birla Institute of Technology and Science Pilani , 
      Jhunjhunu , Pilani , Rajasthan , India.
FAU - Ramagiri, Sruthi
AU  - Ramagiri S
AD  - a Department of Pharmacy , Birla Institute of Technology and Science Pilani , 
      Jhunjhunu , Pilani , Rajasthan , India.
LA  - eng
PT  - Journal Article
DEP - 20151110
PL  - England
TA  - J Recept Signal Transduct Res
JT  - Journal of receptor and signal transduction research
JID - 9509432
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 9FN79X2M3F (Lithium)
RN  - EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta)
SB  - IM
MH  - Animals
MH  - Brain Ischemia/genetics/metabolism/pathology
MH  - Brain-Derived Neurotrophic Factor/*biosynthesis/genetics
MH  - Gene Expression Regulation/drug effects
MH  - Glycogen Synthase Kinase 3 beta/*biosynthesis/genetics
MH  - Humans
MH  - Infarction, Middle Cerebral Artery
MH  - Lithium/*administration & dosage
MH  - Male
MH  - Neuroprotective Agents/administration & dosage
MH  - Oxidative Stress/drug effects
MH  - Rats
MH  - Reperfusion Injury/*genetics/metabolism
MH  - Tumor Necrosis Factor-alpha/*biosynthesis/genetics
OTO - NOTNLM
OT  - BDNF
OT  - GSK-3
OT  - brain
OT  - ischemia reperfusion
OT  - stroke
EDAT- 2015/11/12 06:00
MHDA- 2017/04/05 06:00
CRDT- 2015/11/12 06:00
PHST- 2015/11/12 06:00 [entrez]
PHST- 2015/11/12 06:00 [pubmed]
PHST- 2017/04/05 06:00 [medline]
AID - 10.3109/10799893.2015.1108338 [doi]
PST - ppublish
SO  - J Recept Signal Transduct Res. 2016 Aug;36(4):402-10. doi: 
      10.3109/10799893.2015.1108338. Epub 2015 Nov 10.