• Experimental neurology · Mar 2015

    Fullerenols and glucosamine fullerenes reduce infarct volume and cerebral inflammation after ischemic stroke in normotensive and hypertensive rats.

    • Felix Fluri, Dan Grünstein, Ertugrul Cam, Udo Ungethuem, Florian Hatz, Juliane Schäfer, Samuel Samnick, Ina Israel, Christoph Kleinschnitz, Guillermo Orts-Gil, Holger Moch, Thomas Zeis, Nicole Schaeren-Wiemers, and Peter Seeberger.
    • Department of Neurology, University Hospital Zürich, 8091 Zürich, Switzerland; Department of Neurology, University Hospital Basel, 4031 Basel, Switzerland. Electronic address: felix.fluri@gmx.ch.
    • Exp. Neurol. 2015 Mar 1;265:142-51.

    AbstractCerebral inflammation plays a crucial role in the pathophysiology of ischemic stroke and is involved in all stages of the ischemic cascade. Fullerene derivatives, such as fullerenol (OH-F) are radical scavengers acting as neuroprotective agents while glucosamine (GlcN) attenuates cerebral inflammation after stroke. We created novel glucosamine-fullerene conjugates (GlcN-F) to combine their protective effects and compared them to OH-F regarding stroke-induced cerebral inflammation and cellular damage. Fullerene derivatives or vehicle was administered intravenously in normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) immediately after transient middle cerebral artery occlusion (tMCAO). Infarct size was determined at day 5 and neurological outcome at days 1 and 5 after tMCAO. CD68- and NeuN-staining were performed to determine immunoreactivity and neuronal survival respectively. Cytokine and toll like receptor 4 (TLR-4) expression was assessed using quantitative real-time PCR. Magnetic resonance imaging revealed a significant reduction of infarct volume in both, WKY and SHR that were treated with fullerene derivatives. Treated rats showed an amelioration of neurological symptoms as both OH-F and GlcN-F prevented neuronal loss in the perilesional area. Cerebral immunoreactivity was reduced in treated WKY and SHR. Expression of IL-1β and TLR-4 was attenuated in OH-F-treated WKY rats. In conclusion, OH-F and GlcN-F lead to a reduction of cellular damage and inflammation after stroke, rendering these compounds attractive therapeutics for stroke.Copyright © 2015 Elsevier Inc. All rights reserved.

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