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The Neuroprotective Effect of Cerebrolysin Against Type 1 Diabetes‐Induced Dementia In Rats
Author(s) -
Nassar Noha N,
Georgy Gehan S.,
Mansour Hanaa A.,
Abdallah Dalaal M
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1169.8
Subject(s) - neuroprotection , endocrinology , medicine , hippocampal formation , streptozotocin , diabetes mellitus , hippocampus , neurodegeneration , cerebrolysin , glutamate receptor , disease , receptor
Cognitive decline and increased dementia are associated with diabetes. This work aimed to evaluate the potential neuroprotective effect of cerebrolysin (CBL) in modulating hippocampal alterations associated with streptozotocin (STZ) hyperglycemic complications. To this end, male Sprague Dawley rats were divided into (i) control (ii) CBL control (4 weeks) (iii) STZ diabetic control, and (iv) STZ + CBL (4 weeks). Diabetes was confirmed by hyperglycemia and elevated glycated haemoglobin (HbA1c) % level, which were associated by weight loss, elevation in serum tumor necrosis factor (TNF)‐α and decreased serum insulin like growth factor (IGF)‐1 levels. Furthermore, STZ caused learning and memory impairment that corroborated degenerative changes and neuronal loss in the hippocampus. Behavioral deficit was associated by changes in several neurotransmitter molecules. Moreover, diabetic rats showed an increase in hippocampal nitric oxide as well as thiobarbituric acid derivatives levels, however non‐protein thiols decreased. Though CBL did not affect STZ‐induced hyperglycemia, it partly improved body weight and HbA1c %. Such effects were associated by enhancement in both learning and memory as well as apparent normal cellularity in CA1and CA3 areas. CBL amended serum TNF‐α, IGF‐1, glutamate (GLU), serotonin (5‐HT) as well as oxidative biomarkers In conclusion, CBL possesses neuroprotection against diabetes‐associated cerebral neurodegeneration and cognitive decline via anti‐inflammatory and antioxidant effects as well as modulating hippocampal GLU and 5‐HT.