Original Nerve Growth Factor Mimetic Dipeptide GK-2 Limits the Manifestations of Hemorrhagic Stroke in Rats

Kraineva, V. A.; Gudasheva, T. A.; Kotel'nikova, S O; Антипова, Т. А.; Середенин, С. Б.

doi:10.1007/s10517-013-2020-9

Cited by 3 publications

(2 citation statements)

References 7 publications

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“…In accordance, Ostrovskaya et al have demonstrated a neuroprotective effect of dipeptide in an in-vitro study (30). In this regard, other studies have indicated that dipeptides exhibit neuroprotective properties in various pathological conditions, including traumatic brain injury and hemorrhagic stroke models (31,32). (36).…”

Section: Hasegava Et Al Declared Neurotrophins Has An Important Role ...mentioning

confidence: 66%

A New Dipeptide H-MGL Partially Ameliorates Memory Impairment in an STZ-Induced Alzheimer Model in Male Rats

Ghasempour,

Maghsoudi,

Manaheji

et al. 2023

BCN

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Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is identified by the gradual decline in memory and cognitive function. It is classified by the deposition of Aβ plaques, the build-up of intracellular neurofibrillary tangle and neuron loss. Neurotrophic factors play critical role in the treatment of Alzheimer's disease. However, the utilization of such neurotrophins has encountered certain difficulties and side effects. Novel technological advancements prioritize innovative dipeptides usage, which offer fewer side effects. The present study endeavors to analyze the compound hexamethylenediamide bis-(N-monosuccinyl-glutamyl-lysine) (Lab name: H-MGL), a newly discovered neurotrophin mimetic dipeptide, with the aim of alleviating memory impairment in an intracerebroventricular single dose streptozotocin (STZ)-induced Alzheimer model in rats. We arranged 4 groups consist of sham, groups receiving STZ and STZ+H-MGL (1 and 2mg/kg). The H-MGL was administered consecutively for 14 days following STZ injection subsequently, the Morris Water Maze test was performed. The findings suggest that administration of STZ caused significantly increment in mean escape latency and mean traveled distance in acquisition days. H-MGL at a dosage of 1mg/kg failed to yield any notable improvement in rats when compared to STZ. By contrast, a dosage of 2mg/kg of H-MGL led to a significant decrease in the latency to first platform crossing and frequency of platform crossings. Consequently, the aforementioned findings have engendered the notion that H-MGL partially ameliorate cognitive impairment so it may hold promise for having low side effects to alleviate cognitive deficits in Alzheimer's disease, or potentially decreases the symptoms associated with its progression.

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Section: Hasegava Et Al Declared Neurotrophins Has An Important Role ...mentioning

confidence: 66%

A New Dipeptide H-MGL Partially Ameliorates Memory Impairment in an STZ-Induced Alzheimer Model in Male Rats

Ghasempour,

Maghsoudi,

Manaheji

et al. 2023

BCN

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“…In vivo experiments provided convincing evidence of the GK-2 neuroprotective effects. The efficacy of GK-2 was demonstrated in various models of Alzheimer’s disease (septo-hippocampal transection, cholinergic deficiency caused by prolonged administration of scopolamine, and on a model induced by administration of streptozotocin into the cerebral ventricles [23]), focal and global cerebral ischemia [24], and hemorrhagic stroke [25].…”

Section: Introductionmentioning

confidence: 99%

A Novel Dipeptide NGF Mimetic GK-2 Selectively Activating the PI3K/AKT Signaling Pathway Promotes the Survival of Pancreatic β-Cells in a Rat Model of Diabetes

et al. 2019

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We investigated the cytoprotective effect of a novel low-molecular-weight NGF mimetic, GK-2 (hexamethylenediamide bis-N-monosuccinyl-L-glutamyl-L-lysine), on pancreatic -cells. The neuroprotective effect of GK-2 had been previously shown to be associated with selective activation of the PI3K/Akt signaling pathway. In this study, rats with streptozotocin (STZ)-induced type 2 diabetes mellitus were used. Metformin was used as a reference drug. STZ was immunohistochemically demonstrated to reduce the number of -cells and affect their morphological structure. Treatment of diabetic animals with GK-2 (at a dose of 0.5 mg/kg intraperitoneally or 5 mg/kg orally) or metformin (300 mg/kg orally) for 28 days reduced the damaging effect of STZ. The effect of GK-2 on manifestations of STZ-induced diabetes, such as hyperglycemia, weight loss, polyphagia, and polydipsia, was comparable to that of metformin, while the cytoprotective activity of GK-2 was slightly stronger than that of metformin. A strong positive correlation between morphometric parameters and the blood glucose level was revealed. The GK-2 cytoprotective effect on -cells is supposed to manifest through the PI3K/Akt signaling pathway.

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Innovative Therapy for Alzheimer’s Disease-With Focus on Biodelivery of NGF

2019

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Alzheimer’s disease (AD) is a progressive neurodegenerative disorder associated with abnormal protein modification, inflammation and memory impairment. Aggregated amyloid beta (Aβ) and phosphorylated tau proteins are medical diagnostic features. Loss of memory in AD has been associated with central cholinergic dysfunction in basal forebrain, from where the cholinergic circuitry projects to cerebral cortex and hippocampus. Various reports link AD progression with declining activity of cholinergic neurons in basal forebrain. The neurotrophic molecule, nerve growth factor (NGF), plays a major role in the maintenance of cholinergic neurons integrity and function, both during development and adulthood. Numerous studies have also shown that NGF contributes to the survival and regeneration of neurons during aging and in age-related diseases such as AD. Changes in neurotrophic signaling pathways are involved in the aging process and contribute to cholinergic and cognitive decline as observed in AD. Further, gradual dysregulation of neurotrophic factors like NGF and brain derived neurotrophic factor (BDNF) have been reported during AD development thus intensifying further research in targeting these factors as disease modifying therapies against AD. Today, there is no cure available for AD and the effects of the symptomatic treatment like cholinesterase inhibitors (ChEIs) and memantine are transient and moderate. Although many AD treatment studies are being carried out, there has not been any breakthrough and new therapies are thus highly needed. Long-term effective therapy for alleviating cognitive impairment is a major unmet need. Discussion and summarizing the new advancements of using NGF as a potential therapeutic implication in AD are important. In summary, the intent of this review is describing available experimental and clinical data related to AD therapy, priming to gain additional facts associated with the importance of NGF for AD treatment, and encapsulated cell biodelivery (ECB) as an efficient tool for NGF delivery.

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Original Nerve Growth Factor Mimetic Dipeptide GK-2 Limits the Manifestations of Hemorrhagic Stroke in Rats

Cited by 3 publications

References 7 publications

A New Dipeptide H-MGL Partially Ameliorates Memory Impairment in an STZ-Induced Alzheimer Model in Male Rats

A New Dipeptide H-MGL Partially Ameliorates Memory Impairment in an STZ-Induced Alzheimer Model in Male Rats

A Novel Dipeptide NGF Mimetic GK-2 Selectively Activating the PI3K/AKT Signaling Pathway Promotes the Survival of Pancreatic β-Cells in a Rat Model of Diabetes

Innovative Therapy for Alzheimer’s Disease-With Focus on Biodelivery of NGF

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