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Spatio-temporal course of macrophage-like cell accumulation after experimental embolic stroke depending on treatment with tissue plasminogen activator and its combination with hyperbaric oxygenation

Zitieren Sie bitte immer diese URN: urn:nbn:de:bvb:20-opus-133136
  • Inflammation following ischaemic stroke attracts high priority in current research, particularly using human-like models and long-term observation periods considering translational aspects. The present study aimed on the spatio-temporal course of macrophage-like cell accumulation after experimental thromboembolic stroke and addressed microglial and astroglial reactions in the ischaemic border zone. Further, effects of tissue plasminogen activator (tPA) as currently best treatment for stroke and the potentially neuroprotective co-administrationInflammation following ischaemic stroke attracts high priority in current research, particularly using human-like models and long-term observation periods considering translational aspects. The present study aimed on the spatio-temporal course of macrophage-like cell accumulation after experimental thromboembolic stroke and addressed microglial and astroglial reactions in the ischaemic border zone. Further, effects of tissue plasminogen activator (tPA) as currently best treatment for stroke and the potentially neuroprotective co-administration of hyperbaric oxygen (HBO) were investigated. Rats underwent middle cerebral artery occlusion and were assigned to control, tPA or tPA+HBO. Twenty-four hours, 7, 14 and 28 days were determined as observation time points. The accumulation of macrophage-like cells was semiquantitatively assessed by CD68 staining in the ischaemic area and ischaemic border zone, and linked to the clinical course. CD11b, ionized calcium binding adaptor molecule 1 (Iba), glial fibrillary acidic protein (GFAP) and Neuronal Nuclei (NeuN) were applied to reveal delayed glial and neuronal alterations. In all groups, the accumulation of macrophage-like cells increased distinctly from 24 hours to 7 days post ischaemia. tPA+HBO tended to decrease macrophage-like cell accumulation at day 14 and 28. Overall, a trend towards an association of increased accumulation and pronounced reduction of the neurological deficit was found. Concerning delayed inflammatory reactions, an activation of microglia and astrocytes with co-occurring neuronal loss was observed on day 28. Thereby, astrogliosis was found circularly in contrast to microglial activation directly in the ischaemic area. This study supports previous data on long-lasting inflammatory processes following experimental stroke, and additionally provides region-specific details on glial reactions. The tendency towards a decreasing macrophage-like cell accumulation after tPA+HBO needs to be discussed critically since neuroprotective properties were recently ascribed to long-term inflammatory processes.zeige mehrzeige weniger

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Metadaten
Autor(en): D. Michalski, M. Heindl, J. Kacza, F. Laignel, L. Küppers-Tiedt, D. Schneider, J. Grosche, J. Boltze, M. Löhr, C. Hobohm, W. Härtig
URN:urn:nbn:de:bvb:20-opus-133136
Dokumentart:Artikel / Aufsatz in einer Zeitschrift
Institute der Universität:Medizinische Fakultät / Neurochirurgische Klinik und Poliklinik
Sprache der Veröffentlichung:Englisch
Titel des übergeordneten Werkes / der Zeitschrift (Englisch):European Journal of Histochemistry
Erscheinungsjahr:2012
Band / Jahrgang:56
Heft / Ausgabe:2
Erste Seite:78
Letzte Seite:89
Originalveröffentlichung / Quelle:European Journal of Histochemistry 2012; 56:e14 doi:10.4081/ejh.2012.e14
DOI:https://doi.org/10.4081/ejh.2012.e14
Allgemeine fachliche Zuordnung (DDC-Klassifikation):6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 617 Chirurgie und verwandte medizinische Fachrichtungen
Freie Schlagwort(e):HBO; astroglia; blood-brain-barrier; experimental stroke; focal cerebral-ischemia; inflammatory mechanisms; macrophages; microglia; mononuclear phagocytes; tPA; tumor-necrosis-factor
Datum der Freischaltung:12.01.2017
Lizenz (Deutsch):License LogoCC BY-NC: Creative-Commons-Lizenz: Namensnennung, Nicht kommerziell