Publications by authors named "I P KRASILNIKOVA"

The scratch test is used as an experimental in vitro model of mechanical damage to primary neuronal cultures to study the mechanisms of cell death in damaged areas. The involvement of NMDA receptors in processes leading to delayed neuronal death, due to calcium dysregulation and synchronous mitochondrial depolarization, has been previously demonstrated. In this study, we explored the neuroregenerative potential of Pro-Gly-Pro (PGP)-an endogenous regulatory peptide with neuroprotective and anti-inflammatory properties and a mild chemoattractant effect.

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  • Stem cell technology is pivotal in regenerative medicine, utilizing stem/progenitor cells for repairing or replacing damaged tissues to treat various diseases like cardiovascular and neurological disorders.
  • Cell therapy works through two main mechanisms: the replacement of damaged tissue and the release of biologically active molecules that aid in tissue regeneration, but challenges like transportation complexity and immune rejection exist.
  • The study focuses on the beneficial effects of proteins secreted by glial progenitor cells, showing they can reduce inflammation and support neuron survival by inhibiting harmful factors and maintaining cellular health, potentially paving the way for new therapeutic applications.
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  • Brain injury causes neuroinflammation, high extracellular glutamate levels, and mitochondrial dysfunction, all contributing to neuronal death.
  • The study analyzed patients with aneurysmal subarachnoid hemorrhage and conducted in vitro experiments to investigate the impact of these mechanisms on neuron health.
  • Results indicate that the inhibition of the 2-oxoglutarate dehydrogenase complex by nitric oxide leads to increased extracellular glutamate and subsequent neuronal death, while thiamine can help reverse this toxicity.
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Glutamate excitotoxicity is involved in the pathogenesis of many disorders, including stroke, traumatic brain injury, and Alzheimer's disease, for which central insulin resistance is a comorbid condition. Neurotoxicity of glutamate (Glu) is primarily associated with hyperactivation of the ionotropic N-methyl-D-aspartate receptors (NMDARs), causing a sustained increase in intracellular free calcium concentration ([Ca]) and synchronous mitochondrial depolarization and an increase in intracellular superoxide anion radical (O) production. Recently, we found that insulin protects neurons against excitotoxicity by decreasing the delayed calcium deregulation (DCD).

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In vitro models of traumatic brain injury (TBI) help to elucidate the pathological mechanisms responsible for cell dysfunction and death. To simulate in vitro the mechanical brain trauma, primary neuroglial cultures were scratched during different periods of network formation. Fluorescence microscopy was used to measure changes in intracellular free Ca concentration ([Ca]) and mitochondrial potential (ΔΨm) a few minutes later and on days 3 and 7 after scratching.

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