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      Extended normobaric hyperoxia therapy yields greater neuroprotection for focal transient ischemia-reperfusion in rats

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          Abstract

          Background

          Normobaric hyperoxia (NBO) therapy is neuroprotective in acute ischemic stroke. However, how long the NBO should last to obtain optimal outcome is still unclear. Reports show that ischemic penumbra blood supply may remain compromised for a long period after ischemia-reperfusion, which would impair tissue oxygenation in ischemic penumbra. Therefore, we hypothesized that longer-lasting NBO may yield greater neuroprotection.

          Methods

          The relationship between treatment outcome and NBO duration was examined in this study. Rats were subjected to 90 min middle cerebral artery occlusion followed by reperfusion for 22.5 hours. NBO started at 30 min post ischemia and lasted for 2, 4 or 8 h. Treatment efficacy was evaluated by measuring infarction volume, oxidative stress and apoptosis.

          Results

          Among 2 h, 4 h and 8 h NBO, 8 h NBO offered the greatest efficacy in reducing 24-hour infarction volume, attenuating oxidative stress that was indicated by decreased production of 8-hydroxydeoxyguanosine and NADPH oxidase catalytic subunit gp91 phox, and alleviating apoptosis that was associated with reduced production of DNA fragment and caspase-3 activity in cortex penumbra.

          Conclusions

          Under our experimental conditions, longer duration of NBO treatment produced greater benefits in focal transient cerebral ischemia-reperfusion rats.

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          Most cited references29

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          Activation and cleavage of caspase-3 in apoptosis induced by experimental cerebral ischemia.

          Shobu Namura, Jinmin Zhu, Klaus Fink … (1998)
          We examined the expression, activation, and cellular localization of caspase-3 (CPP32) using immunohistochemistry, immunoblots, and cleavage of the fluorogenic substrate N-benzyloxycarbonyl-Asp-Glu-Val-Asp-7-amino-4-trifluoromethyl coumarin (zDEVD-afc) in adult mouse brain after temporary (2 hr) middle cerebral artery occlusion produced by filament insertion into the carotid artery. Immunoreactive caspase-3p32 but not its cleavage product caspase-3p20 was constitutively expressed in neurons throughout brain and was most prominent in neuronal perikarya within piriform cortex. Caspase-like enzyme activity was elevated in brain homogenate 0-3 hr after reperfusion and reached a peak within 30 to 60 min. Caspase-3p20 immunoreactivity became prominent in neuronal perikarya within the middle cerebral artery territory at the time of reperfusion and on immunoblots 1-12 hr later. DNA laddering (agarose gels) and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL)-stained cells were detected 6-24 hr after reperfusion. At 12-24 hr, immunoreactive p20 was visualized in TUNEL-positive cells, a finding also observed in apoptotic mouse cerebellar granule cells on postnatal day 5. Together, these observations suggest the existence of a time-dependent evolution of ischemic injury characterized by the close correspondence between caspase-like enzyme activation and an associated increase in immunoreactive product (caspase-3p20) beginning at or before reperfusion and followed several hours later by morphological and biochemical features of apoptosis.
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            Edaravone reduces early accumulation of oxidative products and sequential inflammatory responses after transient focal ischemia in mice brain.

            Yoshikuni Mizuno, Takao Urabe, M Komine … (2005)
            Oxidative stress contributes to ischemia/reperfusion neuronal damage in a consecutive 2-phase pattern: an immediate direct cytotoxic effect and subsequent redox-mediated inflammatory insult. The present study was designed to assess the neuroprotective mechanisms of edaravone, a novel free radical scavenger, through antioxidative and anti-inflammatory pathways, from the early period to up to 7 days after ischemia/reperfusion in mice. Mice were subjected to 60-minute ischemia followed by reperfusion. They were divided into the edaravone group (n=72; with different schedules for first administration) and the vehicle (control) group (n=36). Infarct volume and neurological deficit scores were evaluated at several time points after ischemia. Immunohistochemical analysis for 4-hydroxy-2-nonenal (HNE), 8-hydroxy-deoxyguanosine (8-OHdG), ionized calcium-binding adapter molecule 1 (Iba-1), inducible NO synthase (iNOS), and nitrotyrosine were performed at 24 hours, 72 hours, or 7 days after reperfusion. Edaravone, even when administrated 6 hours after onset of ischemia/reperfusion, significantly reduced the infarct volume (68.10+/-6.24%; P<0.05) and improved the neurological deficit scores (P<0.05) at 24 hours after reperfusion. Edaravone markedly suppressed the accumulation of HNE-modified protein and 8-OHdG at the penumbra area during the early period after reperfusion (P<0.05) and reduced microglial activation, iNOS expression, and nitrotyrosine formation at the late period. Our results indicated that edaravone exerts an early neuroprotective effect through the early free radicals scavenging pathway and a late anti-inflammatory effect and suggested that edaravone is important for expansion of the therapeutic time window in stroke patients.
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              Ischemic stroke injury is reduced in mice lacking a functional NADPH oxidase.

              Robert S. Green, Walter C Darbonne, I Rae … (1997)
              Free radicals account for a significant proportion of the brain damage that occurs during ischemic stroke. Using mutant mice (X-CGD) with a dysfunctional phagocytic NADPH oxidase, we investigated the role of this superoxide-generating enzyme as a mediator of the reperfusion injury in a mouse model of middle cerebral artery occlusion. Transient (2 hour) middle cerebral artery occlusion was performed in X-CGD or wild-type litter mates (8- to 10-week-old). After 22 hours of reperfusion, brains were harvested and infarct volume delineated using 2,3,5-triphenyl-tetrazolium chloride. To elucidate the origin of the damaging NADPH oxidase, transient ischemia was also performed in X-CGD or wild-type mice transplanted with wild-type C57 B1/6J or X-CGD bone marrow, respectively. The infarct volume induced by transient ischemia was significantly less in X-CGD mice (29.1 +/- 5.6 mm3; n = 13) than wild-type littermates (54.0 +/- 10.6 mm3; n = 10; P < .05). The elimination of a functional NADPH oxidase from either the circulation or the central nervous system, by performing the appropriate bone marrow transplant experiments, did not reduce the infarct size induced by transient ischemia. This suggests that in order to confer protection against transient ischemia and reperfusion, a putative neuronal and circulating NADPH oxidase need to be inactivated. Brain injury was reduced in mice lacking a functional NADPH oxidase in both the central nervous system and peripheral leukocytes, suggesting a pivotal role for the NADPH oxidase in the pathogenesis of ischemia-reperfusion injury in the brain.
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                Author and article information

                Contributors
                Zhongrui Yuan
                Rong Pan
                Wenlan Liu
                Ke Jian Liu
                Journal
                Journal ID (nlm-ta): Med Gas Res
                Journal ID (iso-abbrev): Med Gas Res
                Title: Medical Gas Research
                Publisher: BioMed Central
                ISSN (Electronic): 2045-9912
                Publication date Collection: 2014
                Publication date (Electronic): 10 August 2014
                Volume: 4
                Page: 14
                Affiliations
                [1 ]College of Pharmacy, University of New Mexico Health Sciences Center, MSC09 5360, Albuquerque, NM 87131-0001, USA
                [2 ]College of Medicine, Shandong University, Jinan 250012, China
                Article
                Publisher ID: 2045-9912-4-14
                DOI: 10.1186/2045-9912-4-14
                PMC ID: 4149308
                PubMed ID: 25177481
                SO-VID: 3e3309cc-a061-4092-8066-6235bd476921
                Copyright © Copyright © 2014 Yuan et al.; licensee BioMed Central Ltd.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 15 April 2014
                Date accepted : 4 August 2014
                Categories
                Subject: Research

                ScienceOpen disciplines: Molecular medicine
                Keywords: apoptosis,ischemic stroke,normobaric hyperoxia,oxidative stress,tissue oxygenation
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: apoptosis, ischemic stroke, normobaric hyperoxia, oxidative stress, tissue oxygenation

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