Open Access
Drug Design, Development and Therapy, volume Volume 10, pages 3545-3553
Mimetics of brain-derived neurotrophic factor loops 1 and 4 are active in a model of ischemic stroke in rats
Publication type: Journal Article
Publication date: 2016-11-02
Journal:
Drug Design, Development and Therapy
Quartile SCImago
Q1
Quartile WOS
Q1
Impact factor: 4.8
ISSN: 11778881
PubMed ID:
27843294
Drug Discovery
Pharmacology
Pharmaceutical Science
Abstract
Background Two dimeric dipeptides, bis-(N-monosuccinyl-l-seryl-l-lysine)hexamethylenediamide (GSB-106) and bis-(N-monosuccinyl-l-methionyl-l-serine) heptamethylenediamide (GSB-214), were designed based on the brain-derived neurotrophic factor (BDNF) loop 4 and loop 1 β-turn sequences, respectively. Earlier, both of these dipeptides were shown to exhibit neuroprotective activity in vitro (10−5–10−8 M). The present study aimed to investigate the mechanisms of action of these peptides and their neuroprotective activity in an experimental stroke model. Methods We used western blot and HT-22 hippocampal neuronal cell line to investigate whether these peptides induced phosphorylation of the TrkB receptor and the AKT and ERK kinases. Rat middle cerebral artery occlusion (MCAO) was used as a stroke model. GSB-106 and GSB-214 were administered intraperitoneally (0.1 mg (1.3×10−7 mol)/kg) 4 hours after MCAO and daily for 7 days. The cerebral infarct volumes were measured with 2,3,5-triphenyltetrazolium chloride staining 21 days after MCAO. Results Both compounds were shown to elevate the TrkB phosphorylation level while having different post-receptor signaling patterns. GSB-106 activated the PI3K/AKT and MAPK/ERK pathways simultaneously, whereas GSB-214 activated the PI3K/AKT only. In experimental stroke, the reduction of cerebral infarct volume by GSB-106 (∼66%) was significantly greater than that of GSB-214 (∼28% reduction), which could be explained by the fundamental role of the MAPK/ERK pathway in neurogenesis and neuroplasticity. Notably, between these two dipeptides, only GSB-106 exhibited antidepressant activity, as was found previously. Conclusion The results provided support for the beneficial pharmacological properties of BDNF loop 4 mimetic GSB-106, thereby suggesting a potential role for this dipeptide as a therapeutic agent.
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Gudasheva T. A. et al. Mimetics of brain-derived neurotrophic factor loops 1 and 4 are active in a model of ischemic stroke in rats // Drug Design, Development and Therapy. 2016. Vol. Volume 10. pp. 3545-3553.
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Gudasheva T. A., Povarnina P., Logvinov I. O., Antipova T. A., Seredenin S. B. Mimetics of brain-derived neurotrophic factor loops 1 and 4 are active in a model of ischemic stroke in rats // Drug Design, Development and Therapy. 2016. Vol. Volume 10. pp. 3545-3553.
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TY - JOUR
DO - 10.2147/DDDT.S118768
UR - https://doi.org/10.2147%2FDDDT.S118768
TI - Mimetics of brain-derived neurotrophic factor loops 1 and 4 are active in a model of ischemic stroke in rats
T2 - Drug Design, Development and Therapy
AU - Gudasheva, Tatyana A
AU - Povarnina, Polina
AU - Logvinov, Ilya O.
AU - Antipova, Tatyana A
AU - Seredenin, Sergey B.
PY - 2016
DA - 2016/11/02 00:00:00
PB - Dove Medical Press
SP - 3545-3553
VL - Volume 10
PMID - 27843294
SN - 1177-8881
ER -
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@article{2016_Gudasheva,
author = {Tatyana A Gudasheva and Polina Povarnina and Ilya O. Logvinov and Tatyana A Antipova and Sergey B. Seredenin},
title = {Mimetics of brain-derived neurotrophic factor loops 1 and 4 are active in a model of ischemic stroke in rats},
journal = {Drug Design, Development and Therapy},
year = {2016},
volume = {Volume 10},
publisher = {Dove Medical Press},
month = {nov},
url = {https://doi.org/10.2147%2FDDDT.S118768},
pages = {3545--3553},
doi = {10.2147/DDDT.S118768}
}
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