PMID- 23840309
OWN - NLM
STAT- MEDLINE
DCOM- 20171031
LR  - 20240313
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 8
IP  - 6
DP  - 2013
TI  - Cerebrolysin Ameloriates Cognitive Deficits in Type III Diabetic Rats.
PG  - e64847
LID - 10.1371/journal.pone.0064847 [doi]
LID - e64847
AB  - Cerebrolysin (CBL), a mixture of several active peptide fragments and 
      neurotrophic factors including brain-derived neurotrophic factor (BDNF), is 
      currently used in the management of cognitive alterations in patients with 
      dementia. Since Cognitive decline as well as increased dementia are strongly 
      associated with diabetes and previous studies addressed the protective effect of 
      BDNF in metabolic syndrome and type 2 diabetes; hence this work aimed to evaluate 
      the potential neuroprotective effect of CBL in modulating the complications of 
      hyperglycaemia experimentally induced by streptozotocin (STZ) on the rat brain 
      hippocampus. To this end, male adult Sprague Dawley rats were divided into (i) 
      vehicle- (ii) CBL- and (iii) STZ diabetic-control as well as (iv) STZ+CBL groups. 
      Diabetes was confirmed by hyperglycemia and elevated glycated haemoglobin 
      (HbA1c%), which were associated by weight loss, elevated tumor necrosis factor 
      (TNF)-alpha and decreased insulin growth factor (IGF)-1beta in the serum. Uncontrolled 
      hyperglycemia caused learning and memory impairments that corroborated 
      degenerative changes, neuronal loss and expression of caspase (Casp)-3 in the 
      hippocampal area of STZ-diabetic rats. Behavioral deficits were associated by 
      decreased hippocampal glutamate (GLU), glycine, serotonin (5-HT) and dopamine. 
      Moreover, diabetic rats showed an increase in hippocampal nitric oxide and 
      thiobarbituric acid reactive substances versus decreased non-protein sulfhydryls. 
      Though CBL did not affect STZ-induced hyperglycemia, it partly improved body 
      weight as well as HbA1c%. Such effects were associated by enhancement in both 
      learning and memory as well as apparent normal cellularity in CA1and CA3 areas 
      and reduced Casp-3 expression. CBL improved serum TNF-alpha and IGF-1beta, GLU and 5-HT 
      as well as hampering oxidative biomarkers. In conclusion, CBL possesses 
      neuroprotection against diabetes-associated cerebral neurodegeneration and 
      cognitive decline via anti-inflammatory, antioxidant and antiapototic effects.
FAU - Georgy, Gehan S
AU  - Georgy GS
AD  - Department of Pharmacology, National Organization of Drug Control and Research 
      (NODCAR), Giza, Egypt.
FAU - Nassar, Noha N
AU  - Nassar NN
FAU - Mansour, Hanaa A
AU  - Mansour HA
FAU - Abdallah, Dalaal M
AU  - Abdallah DM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130619
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Amino Acids)
RN  - 0 (Insulin)
RN  - 0 (Neuroprotective Agents)
RN  - 37KZM6S21G (cerebrolysin)
RN  - 5W494URQ81 (Streptozocin)
SB  - IM
MH  - Amino Acids/*therapeutic use
MH  - Animals
MH  - Brain/drug effects/metabolism
MH  - Cognitive Dysfunction/metabolism/*prevention & control
MH  - Diabetes Mellitus, Experimental/chemically induced/*complications/*drug 
      therapy/*psychology
MH  - Insulin/metabolism
MH  - Male
MH  - Maze Learning/drug effects
MH  - Memory Disorders/metabolism/prevention & control
MH  - Neuroprotective Agents/therapeutic use
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Streptozocin
PMC - PMC3686810
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2013/07/11 06:00
MHDA- 2013/07/11 06:01
PMCR- 2013/06/19
CRDT- 2013/07/11 06:00
PHST- 2012/12/21 00:00 [received]
PHST- 2013/04/19 00:00 [accepted]
PHST- 2013/07/11 06:00 [entrez]
PHST- 2013/07/11 06:00 [pubmed]
PHST- 2013/07/11 06:01 [medline]
PHST- 2013/06/19 00:00 [pmc-release]
AID - PONE-D-13-00121 [pii]
AID - 10.1371/journal.pone.0064847 [doi]
PST - epublish
SO  - PLoS One. 2013 Jun 19;8(6):e64847. doi: 10.1371/journal.pone.0064847. Print 2013.