Year-end Sale % OFF 
Abstract
Therapies against stroke can restore the blood supply but cannot prevent the ischemic damage nor stimulate the recovery of the infarcted zone. The neuroglobin protein plays an important role in the neuro-regeneration process after stroke; however, the method for its effective systemic application has not been identified yet, as neuroglobin is unable to pass through the blood-brain barrier. Previously, we developed different types of sodium hyaluronate nanoparticles, which successfully cross the blood-brain barrier after stroke. In this work, these nanoparticles have been used to carry neuroglobin through the bloodstream to the nerve cells in rats submitted to stroke. We have biosynthesized rat-recombinant neuroglobin and determined the formulation of sodium hyaluronate nanoparticles loaded with neuroglobin, as well as its size and ζ-potential, encapsulation efficiently, in vitro release, and its kinetic of liberation. The results show that the formulation achieved is highly compatible with pharmaceutical use and may act as a delivery system to transport neuroglobin within the blood. We have found that this formulation injected intravenously immediately after stroke reached the damaged cerebral parenchyma at early stages (2 h). Neuroglobin colocalizes with its nanocarriers inside the nerve cells and remains after 24 h of reperfusion. In conclusion, the systemic administration of neuroglobin linked to nanoparticles is a potential neuroprotective drug-delivery strategy after stroke episodes.
Highlights
Stroke is a leading cause of death and long-term disability worldwide [1,2]
According to the information previously provided by other authors [45], NPs with a size between 100 and 200 nm were captured by endocytosis, and particles greater than 300 nm were captured by phagocytosis [45]; the ideal size of the NPs linked to neuroglobin protein (NGB) should be below 300 nm
According to the data analyzed, this size must be a consequence of NGB, which exerts a clear influence on this parameter with respect to the average size of the NPs without the drug, as we have previously published [25]
Summary
Ischemic stroke occurring in the zone irrigated by the middle cerebral artery, it can affect the parietal cortex and striatum, which suffer an energetic unbalance leading to neuronal and glial damage and even to cell death [3]. Current treatments, thrombolysis and thrombectomy are not effective enough due to the narrow therapeutic window and complexity of administration [5,6,7] None of these treatments provide neuroprotection to the ischemic tissue damaged during the reperfusion period. Upregulation of NGB does not appear until 48–72 h of reperfusion after the ischemic insult [21,22] These data, together with NGB being expressed at physiological levels, do not enable resistance to neuronal death following ischemia [23,24]. Rapidly increasing NGB in the penumbra zone of the infarct could change the prognosis of stroke
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
