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      Normobaric Oxygen (NBO) Therapy Reduces Cerebral Ischemia/Reperfusion Injury through Inhibition of Early Autophagy

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          Abstract

          Objectives

          Normobaric oxygen (NBO) therapy has great clinical potential in the treatment of ischemic stroke, but its underlying mechanism is unknown. Our study aimed to investigate the role of autophagy during the application of NBO on cerebral ischemia/reperfusion injury.

          Methods

          Male Sprague Dawley rats received 2 hours of middle cerebral artery occlusion (MCAO), followed by 2, 6, or 24 hours of reperfusion. At the beginning of reperfusion, rats were randomly given NBO (95% O 2) or room air (21% O 2) for 2 hours. In some animals, 3-methyladenine (3-MA, autophagy inhibitor) was administered 10 minutes before reperfusion. The severity of the ischemic injury was determined by infarct volume, neurological deficit, and apoptotic cell death. Western blotting was used to determine the protein expression of autophagy and apoptosis, while mRNA expression of apoptotic molecules was detected by real-time PCR.

          Results

          NBO treatment after ischemia/reperfusion significantly decreased infarct volume and neurobehavioral defects. The increased expression of the autophagy markers, including microtubule-associated protein 1A light chain 3 (LC3) and Beclin 1, after ischemia/reperfusion was reversed by NBO, while promoting Sequestosome 1 (p62/SQSTM1) expression. In addition, NBO reduced cerebral apoptosis in association with alleviated BAX expression and increased BCL-2 expression. 3-MA reduced autophagy and apoptotic death but did not further improve NBO-attenuated ischemic damage.

          Conclusion

          NBO induced remarkable neuroprotection from ischemic injury, which was correlated with blocked autophagy activity.

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          Most cited references53

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          Cell death: a review of the major forms of apoptosis, necrosis and autophagy

          Cell death was once believed to be the result of one of two distinct processes, apoptosis (also known as programmed cell death) or necrosis (uncontrolled cell death); in recent years, however, several other forms of cell death have been discovered highlighting that a cell can die via a number of differing pathways. Apoptosis is characterised by a number of characteristic morphological changes in the structure of the cell, together with a number of enzyme-dependent biochemical processes. The result being the clearance of cells from the body, with minimal damage to surrounding tissues. Necrosis, however, is generally characterised to be the uncontrolled death of the cell, usually following a severe insult, resulting in spillage of the contents of the cell into surrounding tissues and subsequent damage thereof. Failure of apoptosis and the resultant accumulation of damaged cells in the body can result in various forms of cancer. An understanding of the pathways is therefore important in developing efficient chemotherapeutics. It has recently become clear that there exists a number of subtypes of apoptosis and that there is an overlap between apoptosis, necrosis and autophagy. The goal of this review is to provide a general overview of the current knowledge relating to the various forms of cell death, including apoptosis, necrosis, oncosis, pyroptosis and autophagy. This will provide researchers with a summary of the major forms of cell death and allow them to compare and contrast between them.
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            An overview of autophagy: morphology, mechanism, and regulation.

            Autophagy is a highly conserved eukaryotic cellular recycling process. Through the degradation of cytoplasmic organelles, proteins, and macromolecules, and the recycling of the breakdown products, autophagy plays important roles in cell survival and maintenance. Accordingly, dysfunction of this process contributes to the pathologies of many human diseases. Extensive research is currently being done to better understand the process of autophagy. In this review, we describe current knowledge of the morphology, molecular mechanism, and regulation of mammalian autophagy. At the mechanistic and regulatory levels, there are still many unanswered questions and points of confusion that have yet to be resolved. Through further research, a more complete and accurate picture of the molecular mechanism and regulation of autophagy will not only strengthen our understanding of this significant cellular process, but will aid in the development of new treatments for human diseases in which autophagy is not functioning properly.
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              • Article: not found

              Reversible middle cerebral artery occlusion without craniectomy in rats

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                Author and article information

                Contributors
                Journal
                Evid Based Complement Alternat Med
                Evid Based Complement Alternat Med
                ECAM
                Evidence-based Complementary and Alternative Medicine : eCAM
                Hindawi
                1741-427X
                1741-4288
                2021
                30 June 2021
                30 June 2021
                : 2021
                : 7041290
                Affiliations
                1China-America Institute of Neuroscience, Beijing Luhe Hospital, Capital Medical University, Beijing, China
                2Department of Neurology, Beijing Luhe Hospital, Capital Medical University, Beijing, China
                3Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI, USA
                4Drexel University College of Medicine, Philadelphia, PA, USA
                5Department of Research and Development Center, John D. Dingell VA Medical Center, Detroit, MI, USA
                Author notes

                Academic Editor: Elisha R. Injeti

                Author information
                https://orcid.org/0000-0001-6174-4888
                https://orcid.org/0000-0001-8918-8748
                https://orcid.org/0000-0002-7128-6005
                https://orcid.org/0000-0002-1547-7560
                https://orcid.org/0000-0003-0699-9807
                Article
                10.1155/2021/7041290
                8263229
                422113b7-7523-4bde-96b0-c53b41b153f8
                Copyright © 2021 Meng Wang et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 27 April 2021
                : 31 May 2021
                : 20 June 2021
                Funding
                Funded by: National Natural Science Foundation of China
                Award ID: 81871838
                Award ID: 82072549
                Funded by: Science and Technology Plan of Beijing Tongzhou District
                Award ID: KJ2020CX002
                Funded by: Natural Science Foundation of Beijing Municipality
                Award ID: 7214239
                Categories
                Research Article

                Complementary & Alternative medicine
                Complementary & Alternative medicine

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