Neuroprotective Effects of Isosteviol Sodium in Murine Brain Capillary Cerebellar Endothelial Cells (cerebEND) After Hypoxia
Ischemic stroke is one of the leading causes of death worldwide. It damages neurons and other supporting cellular elements in the brain. However, the impairment is not only confined to the region of assault but the surrounding area as well. In addition, it also brings about damage to the blood brain...
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Published in | Frontiers in cellular neuroscience Vol. 14; p. 573950 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
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28.10.2020
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Abstract | Ischemic stroke is one of the leading causes of death worldwide. It damages neurons and other supporting cellular elements in the brain. However, the impairment is not only confined to the region of assault but the surrounding area as well. In addition, it also brings about damage to the blood brain barrier (BBB) which in turn leads to microvascular failure and edema. Hence, this necessitates an on-going, continuous search for intervention strategies and effective treatment.Of late, the natural sweetener stevioside proved to exhibit neuroprotective effects and therapeutic benefits against cerebral-ischemia induced injury. Its injectable formulation, isosteviolsodium (STVNa) also demonstrated favorable results. Nonetheless, its effects on the BBB have not yet been investigated to date. As such, this present study was designed to assess the effects of STVNa in our in vitro stroke model of the BBB.The integrity and permeability of the BBB are governed and maintained by tight junction proteins (TJPs) such as claudin-5 and occludin. Our data show increased claudin-5 and occludin expression in oxygen and glucose (OGD)-deprived murine brain capillary cerebellar endothelial cells (cerebEND) after STVNa treatment. Likewise, upregulation of the transmembrane protein integrin-v was also observed. Finally, cell volume was reduced with simultaneous administration of STVNa and OGD in cerebEND cells.In neuropathologies such as stroke, the failure of cell volume control is a major feature leading to loss of cells in the penumbra as well as adverse outcomes. Our initial findings therefore point to the neuroprotective effects of STVNa at the BBB in vitro, which warrant further investigation for a possible future clinical intervention. |
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AbstractList | Ischemic stroke is one of the leading causes of death worldwide. It damages neurons and other supporting cellular elements in the brain. However, the impairment is not only confined to the region of assault but the surrounding area as well. Besides, it also brings about damage to the blood-brain barrier (BBB) which in turn leads to microvascular failure and edema. Hence, this necessitates an on-going, continuous search for intervention strategies and effective treatment. Of late, the natural sweetener stevioside proved to exhibit neuroprotective effects and therapeutic benefits against cerebral ischemia-induced injury. Its injectable formulation, isosteviol sodium (STVNA) also demonstrated favorable results. Nonetheless, its effects on the BBB have not yet been investigated to date. As such, this present study was designed to assess the effects of STVNA in our
in vitro
stroke model of the BBB.The integrity and permeability of the BBB are governed and maintained by tight junction proteins (TJPs) such as claudin-5 and occludin. Our data show increased claudin-5 and occludin expression in oxygen and glucose (OGD)-deprived murine brain capillary cerebellar endothelial cells (cerebEND) after STVNa treatment. Likewise, the upregulation of the transmembrane protein integrin-αv was also observed. Finally, cell volume was reduced with the simultaneous administration of STVNA and OGD in cerebEND cells. In neuropathologies such as stroke, the failure of cell volume control is a major feature leading to loss of cells in the penumbra as well as adverse outcomes. Our initial findings, therefore, point to the neuroprotective effects of STVNA at the BBB
in vitro
, which warrant further investigation for a possible future clinical intervention. Ischemic stroke is one of the leading causes of death worldwide. It damages neurons and other supporting cellular elements in the brain. However, the impairment is not only confined to the region of assault but the surrounding area as well. Besides, it also brings about damage to the blood-brain barrier (BBB) which in turn leads to microvascular failure and edema. Hence, this necessitates an on-going, continuous search for intervention strategies and effective treatment. Of late, the natural sweetener stevioside proved to exhibit neuroprotective effects and therapeutic benefits against cerebral ischemia-induced injury. Its injectable formulation, isosteviol sodium (STVNA) also demonstrated favorable results. Nonetheless, its effects on the BBB have not yet been investigated to date. As such, this present study was designed to assess the effects of STVNA in our in vitro stroke model of the BBB.The integrity and permeability of the BBB are governed and maintained by tight junction proteins (TJPs) such as claudin-5 and occludin. Our data show increased claudin-5 and occludin expression in oxygen and glucose (OGD)-deprived murine brain capillary cerebellar endothelial cells (cerebEND) after STVNa treatment. Likewise, the upregulation of the transmembrane protein integrin-αv was also observed. Finally, cell volume was reduced with the simultaneous administration of STVNA and OGD in cerebEND cells. In neuropathologies such as stroke, the failure of cell volume control is a major feature leading to loss of cells in the penumbra as well as adverse outcomes. Our initial findings, therefore, point to the neuroprotective effects of STVNA at the BBB in vitro, which warrant further investigation for a possible future clinical intervention. Ischemic stroke is one of the leading causes of death worldwide. It damages neurons and other supporting cellular elements in the brain. However, the impairment is not only confined to the region of assault but the surrounding area as well. In addition, it also brings about damage to the blood brain barrier (BBB) which in turn leads to microvascular failure and edema. Hence, this necessitates an on-going, continuous search for intervention strategies and effective treatment.Of late, the natural sweetener stevioside proved to exhibit neuroprotective effects and therapeutic benefits against cerebral-ischemia induced injury. Its injectable formulation, isosteviolsodium (STVNa) also demonstrated favorable results. Nonetheless, its effects on the BBB have not yet been investigated to date. As such, this present study was designed to assess the effects of STVNa in our in vitro stroke model of the BBB.The integrity and permeability of the BBB are governed and maintained by tight junction proteins (TJPs) such as claudin-5 and occludin. Our data show increased claudin-5 and occludin expression in oxygen and glucose (OGD)-deprived murine brain capillary cerebellar endothelial cells (cerebEND) after STVNa treatment. Likewise, upregulation of the transmembrane protein integrin-v was also observed. Finally, cell volume was reduced with simultaneous administration of STVNa and OGD in cerebEND cells.In neuropathologies such as stroke, the failure of cell volume control is a major feature leading to loss of cells in the penumbra as well as adverse outcomes. Our initial findings therefore point to the neuroprotective effects of STVNa at the BBB in vitro, which warrant further investigation for a possible future clinical intervention. |
Author | Soukhoroukov, Vladimir Förster, Carola Burek, Malgorzata Rösing, Nils Güntzel, Paul Kempe, Christoph Wunder, Christian Salvador, Ellaine Holzgrabe, Ulrike |
AuthorAffiliation | 1 Department of Anesthesia and Critical Care, Division Molecular Medicine, University of Würzburg , Würzburg , Germany 5 Department of Anesthesia and Intensive Care Medicine, Robert-Bosch Hospital , Stuttgart , Germany 2 Tumor Biology Laboratory, Department of Neurosurgery, University of Würzburg , Würzburg , Germany 3 Institute of Pharmacy and Food Chemistry, Biocenter, University of Würzburg , Würzburg , Germany 4 Department of Biotechnology and Biophysics, Biocenter, University of Würzburg , Würzburg , Germany |
AuthorAffiliation_xml | – name: 1 Department of Anesthesia and Critical Care, Division Molecular Medicine, University of Würzburg , Würzburg , Germany – name: 2 Tumor Biology Laboratory, Department of Neurosurgery, University of Würzburg , Würzburg , Germany – name: 4 Department of Biotechnology and Biophysics, Biocenter, University of Würzburg , Würzburg , Germany – name: 5 Department of Anesthesia and Intensive Care Medicine, Robert-Bosch Hospital , Stuttgart , Germany – name: 3 Institute of Pharmacy and Food Chemistry, Biocenter, University of Würzburg , Würzburg , Germany |
Author_xml | – sequence: 1 givenname: Nils surname: Rösing fullname: Rösing, Nils – sequence: 2 givenname: Ellaine surname: Salvador fullname: Salvador, Ellaine – sequence: 3 givenname: Paul surname: Güntzel fullname: Güntzel, Paul – sequence: 4 givenname: Christoph surname: Kempe fullname: Kempe, Christoph – sequence: 5 givenname: Malgorzata surname: Burek fullname: Burek, Malgorzata – sequence: 6 givenname: Ulrike surname: Holzgrabe fullname: Holzgrabe, Ulrike – sequence: 7 givenname: Vladimir surname: Soukhoroukov fullname: Soukhoroukov, Vladimir – sequence: 8 givenname: Christian surname: Wunder fullname: Wunder, Christian – sequence: 9 givenname: Carola surname: Förster fullname: Förster, Carola |
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CitedBy_id | crossref_primary_10_1158_0008_5472_CAN_22_0887 crossref_primary_10_3389_fnmol_2021_745066 crossref_primary_10_3389_fddev_2022_1027098 crossref_primary_10_3389_fnins_2021_649982 crossref_primary_10_3390_antiox11081447 crossref_primary_10_3390_pharmaceutics14091753 crossref_primary_10_2147_JIR_S344990 crossref_primary_10_3390_biom12101452 crossref_primary_10_4103_1673_5374_343896 crossref_primary_10_1016_j_intimp_2022_109532 crossref_primary_10_1016_j_foodchem_2024_139654 |
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Snippet | Ischemic stroke is one of the leading causes of death worldwide. It damages neurons and other supporting cellular elements in the brain. However, the... |
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SubjectTerms | Blood-brain barrier Brain Brain injury Cell culture Cell size Cellular Neuroscience Cerebellum cerebEND cells Cytotoxicity Edema Endothelial cells Gene expression Glucose Hypoxia Ischemia isosteviol sodium Membrane permeability Microvasculature Neuroprotection Permeability Proteins Stevioside Stroke |
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Title | Neuroprotective Effects of Isosteviol Sodium in Murine Brain Capillary Cerebellar Endothelial Cells (cerebEND) After Hypoxia |
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