ArticleNeurochemical research2001
Protective effect of a new hypothalamic peptide against cobra venom and trauma-induced neuronal injury.
Article in Neurochemical research, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 27 citations in OpenAlex.
- Tyrosine-Peptide Analog Modulates Extracellular Vesicles miRNAs Cargo from Mesenchymal Stem/Stromal and Cancer Cells to Drive Immunoregeneration and Tumor Suppression.Biomolecules · 2026Article
- Protective effects of hypothalamic proline-rich peptide and cobra venom Naja Naja Oxiana on dynamics of vestibular compensation following unilateral labyrinthectomy.Neurochemical research · 2010Article
- Hypothalamic proline rich polypeptide regulates hematopoiesis.Neurochemical research · 2010Article
- Effect of hypothalamic proline-rich peptide (PRP-1) on neuronal and bone marrow cell apoptosis.Neurochemical research · 2007Article
- The protective effect of vipera raddei venom on peripheral nerve damage.Neuroscience and behavioral physiology · 2006Article
- PRP-1 protective effect against central and peripheral neurodegeneration following n. ischiadicus transection.Neurochemical research · 2005Article
- Neuroprotective action of hypothalamic peptide PRP-1 at various time survivals following spinal cord hemisection.Neurochemical research · 2005Article
- Hypothalamic proline-rich polypeptide protects brain neurons in aluminum neurotoxicosis.Neurochemical research · 2004Article
- Survival of trauma-injured neurons in rat brain by treatment with proline-rich peptide (PRP-1): an immunohistochemical study.Neurochemical research · 2004Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A study of separate and combined actions of cobra venom (CV) and a new hypothalamic proline-rich polypeptide (PRP) isolated from magnocellular cells (NPV and NSO) on intoxication- and trauma-induced neuronal injury (during 3-4 weeks after hemisection with and without PRP treatment) was carried out. The registration of background and evoked impulse activity flow, changes in spinal cord (SC) inter- and motoneurons, responding to flexor, extensor, and mixed nerve stimulation in both acute and chronic experimental neurodegeneration was performed. The facilitating effect of PRP on the abovementioned neurons was revealed. High doses of CV that evoked the neurodegenerative changes demonstrated an inhibitory effect. In this case PRP treatment both before and after intoxication restored electrical neuronal activity to baseline level and higher. These results are evidence of protective action of PRP. The low doses of CV induced a facilitating effect. The combination of CV and PRP displayed an additive facilitating effect; in a number of cases the repeated administration of CV led to decrease of significant PRP effect till baseline level (for example, the inhibition after primary response prior to secondary late discharge). Greater liability of the secondary early and late long-time discharges of poststimulus responses, differently expressed in various neuron types of SC to chemical influences is of interest. PRP-induced inhibition of the paroxysmal activity related with CV action is also very interesting. Morpho-functional experiments with SC injury demonstrated the abolition of difference in the background and evoked SC neuronal activity below the section and on intact symmetric side after daily PRP administration for 3 weeks. PRP hindered the scar formation and activated neuroglia proliferation; it promoted white matter element growth, hampered the degeneration of cellular elements, and protected against tissue stress. Our results favor the combined use of PRP and CV in clinical practice for the treatment of neurodegeneration of toxic and traumatic origin, as well as specific neurodegenerative diseases such as Alzheimer's.
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