PMID- 30369869
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 1662-5099 (Print)
IS  - 1662-5099 (Electronic)
IS  - 1662-5099 (Linking)
VI  - 11
DP  - 2018
TI  - Antidepressant-Like Effects of Low- and High-Molecular Weight FGF-2 on Chronic 
      Unpredictable Mild Stress Mice.
PG  - 377
LID - 10.3389/fnmol.2018.00377 [doi]
LID - 377
AB  - The occurrence of depressive disorder has long been attributed to changes in 
      monoamines, with the focus of drug treatment strategies being to change the 
      effectiveness of monoamines. However, the success achieved by changing these 
      processes is limited and further stimulates the exploration of alternative 
      mechanisms and treatments. Fibroblast growth factor 2 (FGF-2), which occurs in a 
      high-molecular weight (HMW) and low-molecular weight (LMW) form, is a potent 
      developmental modulator and nervous system regulator that has been suggested to 
      play an important role in various psychiatric disorders. In this study, we 
      investigated the antidepressant effects of HMW and LMW FGF-2 on depression 
      induced by chronic stress. Both peripheral LMW and HMW FGF-2 attenuated the 
      depression-like behaviors in chronic unpredictable mild stress (CUMS) mice to a 
      similar extent, as determined by the forced swimming, tail suspension, and 
      sucrose preference tests. We then showed that CUMS-induced oxidative stresses in 
      mice were inhibited by FGF-2 treatments both in central and peripheral. We also 
      showed that both forms of FGF-2 increased the phosphorylation of ERK and AKT, 
      increased Bcl-2 expression and inhibited caspase-3 activation in CUMS mice. 
      Interestingly, HMW FGF-2 enhanced the activity of the brain-derived neurotrophic 
      factor (BDNF) to a greater extent than did LMW FGF-2 in the hippocampus. Taken 
      together, these results suggest that depressive symptoms can be relieved by 
      administering different forms of FGF-2 peripherally in a CUMS-induced depression 
      model through a similar antidepressant signaling pathway, therefore suggesting a 
      potential clinical use for FGF-2 as a treatment for depression.
FAU - Wang, Lin
AU  - Wang L
AD  - Key Laboratory of Ethnomedicine for Ministry of Education, Center on 
      Translational Neuroscience, College of Life and Environmental Sciences, Minzu 
      University of China, Beijing, China.
FAU - Li, Xi-Xi
AU  - Li XX
AD  - Key Laboratory of Ethnomedicine for Ministry of Education, Center on 
      Translational Neuroscience, College of Life and Environmental Sciences, Minzu 
      University of China, Beijing, China.
FAU - Chen, Xi
AU  - Chen X
AD  - School of Pharmacy, Minzu University of China, Beijing, China.
FAU - Qin, Xiao-Yan
AU  - Qin XY
AD  - Key Laboratory of Ethnomedicine for Ministry of Education, Center on 
      Translational Neuroscience, College of Life and Environmental Sciences, Minzu 
      University of China, Beijing, China.
FAU - Kardami, Elissavet
AU  - Kardami E
AD  - Institute of Cardiovascular Sciences, St. Boniface Hospital Albrechtsen Research 
      Centre, University of Manitoba, Winnipeg, MB, Canada.
FAU - Cheng, Yong
AU  - Cheng Y
AD  - Key Laboratory of Ethnomedicine for Ministry of Education, Center on 
      Translational Neuroscience, College of Life and Environmental Sciences, Minzu 
      University of China, Beijing, China.
LA  - eng
PT  - Journal Article
DEP - 20181012
PL  - Switzerland
TA  - Front Mol Neurosci
JT  - Frontiers in molecular neuroscience
JID - 101477914
PMC - PMC6194172
OTO - NOTNLM
OT  - AKT
OT  - Bcl-2
OT  - Caspase-3
OT  - ERK
OT  - HMW FGF-2
OT  - LMW FGF-2
OT  - depression
OT  - oxidative stress
EDAT- 2018/10/30 06:00
MHDA- 2018/10/30 06:01
PMCR- 2018/01/01
CRDT- 2018/10/30 06:00
PHST- 2018/05/24 00:00 [received]
PHST- 2018/09/21 00:00 [accepted]
PHST- 2018/10/30 06:00 [entrez]
PHST- 2018/10/30 06:00 [pubmed]
PHST- 2018/10/30 06:01 [medline]
PHST- 2018/01/01 00:00 [pmc-release]
AID - 10.3389/fnmol.2018.00377 [doi]
PST - epublish
SO  - Front Mol Neurosci. 2018 Oct 12;11:377. doi: 10.3389/fnmol.2018.00377. 
      eCollection 2018.