Neuroprotective Effects of Cannabidiol Under Cerebral Ischemic Conditions
Abstract The lack of blood flow during cerebral ischemic conditions results in multiple and intricate pathophysiological mechanisms including excitotoxicity, oxidative stress, neuroinflammation, white matter injury, and blood–brain barrier impairment. Despite numerous experimental studies that have...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Meyer, Erika [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2021 |
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| Schlagwörter: |
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| Anmerkung: |
© The Author(s) under exclusive licence to Sociedade Brasileira de Farmacognosia 2021 |
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| Übergeordnetes Werk: |
Enthalten in: Revista Brasileira de farmacognosia - Critiba : Soc. Brasileira de Farmacognosia, 1986, 31(2021), 5 vom: Okt., Seite 579-591 |
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| Übergeordnetes Werk: |
volume:31 ; year:2021 ; number:5 ; month:10 ; pages:579-591 |
| Links: |
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| DOI / URN: |
10.1007/s43450-021-00199-6 |
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| Katalog-ID: |
SPR045966397 |
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| 520 | |a Abstract The lack of blood flow during cerebral ischemic conditions results in multiple and intricate pathophysiological mechanisms including excitotoxicity, oxidative stress, neuroinflammation, white matter injury, and blood–brain barrier impairment. Despite numerous experimental studies that have been conducted in preclinical settings, current treatments for cerebral ischemia including mechanical and pharmacological therapies are limited, and often accompanied by significant side effects. Therefore, it is necessary to investigate new strategies for treating these conditions. Cannabidiol, the most abundant non-psychotomimetic compound obtained from Cannabis sativa L., Cannabaceae, is a pleiotropic compound acting in a variety of molecular targets and may affect many pathophysiological processes resulting in improvement of cerebral ischemia outcomes. In this review, we summarize the main effects of cannabidiol in different animal models of cerebral ischemia and discuss some of its putative mechanisms of neuroprotection. Graphical Abstract | ||
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| 650 | 4 | |a Cannabinoids |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Cerebral blood flow |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Impaired blood flow |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Marijuana |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Neuroprotection |7 (dpeaa)DE-He213 | |
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| 700 | 1 | |a Kirchhoff, Frank |0 (orcid)0000-0002-2324-2761 |4 aut | |
| 700 | 1 | |a de Oliveira, Rúbia Maria Weffort |0 (orcid)0000-0002-6181-1881 |4 aut | |
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10.1007/s43450-021-00199-6 doi (DE-627)SPR045966397 (SPR)s43450-021-00199-6-e DE-627 ger DE-627 rakwb eng Meyer, Erika verfasserin (orcid)0000-0002-8425-6358 aut Neuroprotective Effects of Cannabidiol Under Cerebral Ischemic Conditions 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) under exclusive licence to Sociedade Brasileira de Farmacognosia 2021 Abstract The lack of blood flow during cerebral ischemic conditions results in multiple and intricate pathophysiological mechanisms including excitotoxicity, oxidative stress, neuroinflammation, white matter injury, and blood–brain barrier impairment. Despite numerous experimental studies that have been conducted in preclinical settings, current treatments for cerebral ischemia including mechanical and pharmacological therapies are limited, and often accompanied by significant side effects. Therefore, it is necessary to investigate new strategies for treating these conditions. Cannabidiol, the most abundant non-psychotomimetic compound obtained from Cannabis sativa L., Cannabaceae, is a pleiotropic compound acting in a variety of molecular targets and may affect many pathophysiological processes resulting in improvement of cerebral ischemia outcomes. In this review, we summarize the main effects of cannabidiol in different animal models of cerebral ischemia and discuss some of its putative mechanisms of neuroprotection. Graphical Abstract Animal models (dpeaa)DE-He213 Cannabinoids (dpeaa)DE-He213 Cerebral blood flow (dpeaa)DE-He213 Impaired blood flow (dpeaa)DE-He213 Marijuana (dpeaa)DE-He213 Neuroprotection (dpeaa)DE-He213 de Mattos, Bianca Andretto (orcid)0000-0002-6325-1064 aut Kirchhoff, Frank (orcid)0000-0002-2324-2761 aut de Oliveira, Rúbia Maria Weffort (orcid)0000-0002-6181-1881 aut Enthalten in Revista Brasileira de farmacognosia Critiba : Soc. Brasileira de Farmacognosia, 1986 31(2021), 5 vom: Okt., Seite 579-591 (DE-627)730275531 (DE-600)2690840-2 1981-528X nnns volume:31 year:2021 number:5 month:10 pages:579-591 https://dx.doi.org/10.1007/s43450-021-00199-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 31 2021 5 10 579-591 |
| spelling |
10.1007/s43450-021-00199-6 doi (DE-627)SPR045966397 (SPR)s43450-021-00199-6-e DE-627 ger DE-627 rakwb eng Meyer, Erika verfasserin (orcid)0000-0002-8425-6358 aut Neuroprotective Effects of Cannabidiol Under Cerebral Ischemic Conditions 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) under exclusive licence to Sociedade Brasileira de Farmacognosia 2021 Abstract The lack of blood flow during cerebral ischemic conditions results in multiple and intricate pathophysiological mechanisms including excitotoxicity, oxidative stress, neuroinflammation, white matter injury, and blood–brain barrier impairment. Despite numerous experimental studies that have been conducted in preclinical settings, current treatments for cerebral ischemia including mechanical and pharmacological therapies are limited, and often accompanied by significant side effects. Therefore, it is necessary to investigate new strategies for treating these conditions. Cannabidiol, the most abundant non-psychotomimetic compound obtained from Cannabis sativa L., Cannabaceae, is a pleiotropic compound acting in a variety of molecular targets and may affect many pathophysiological processes resulting in improvement of cerebral ischemia outcomes. In this review, we summarize the main effects of cannabidiol in different animal models of cerebral ischemia and discuss some of its putative mechanisms of neuroprotection. Graphical Abstract Animal models (dpeaa)DE-He213 Cannabinoids (dpeaa)DE-He213 Cerebral blood flow (dpeaa)DE-He213 Impaired blood flow (dpeaa)DE-He213 Marijuana (dpeaa)DE-He213 Neuroprotection (dpeaa)DE-He213 de Mattos, Bianca Andretto (orcid)0000-0002-6325-1064 aut Kirchhoff, Frank (orcid)0000-0002-2324-2761 aut de Oliveira, Rúbia Maria Weffort (orcid)0000-0002-6181-1881 aut Enthalten in Revista Brasileira de farmacognosia Critiba : Soc. Brasileira de Farmacognosia, 1986 31(2021), 5 vom: Okt., Seite 579-591 (DE-627)730275531 (DE-600)2690840-2 1981-528X nnns volume:31 year:2021 number:5 month:10 pages:579-591 https://dx.doi.org/10.1007/s43450-021-00199-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 31 2021 5 10 579-591 |
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10.1007/s43450-021-00199-6 doi (DE-627)SPR045966397 (SPR)s43450-021-00199-6-e DE-627 ger DE-627 rakwb eng Meyer, Erika verfasserin (orcid)0000-0002-8425-6358 aut Neuroprotective Effects of Cannabidiol Under Cerebral Ischemic Conditions 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) under exclusive licence to Sociedade Brasileira de Farmacognosia 2021 Abstract The lack of blood flow during cerebral ischemic conditions results in multiple and intricate pathophysiological mechanisms including excitotoxicity, oxidative stress, neuroinflammation, white matter injury, and blood–brain barrier impairment. Despite numerous experimental studies that have been conducted in preclinical settings, current treatments for cerebral ischemia including mechanical and pharmacological therapies are limited, and often accompanied by significant side effects. Therefore, it is necessary to investigate new strategies for treating these conditions. Cannabidiol, the most abundant non-psychotomimetic compound obtained from Cannabis sativa L., Cannabaceae, is a pleiotropic compound acting in a variety of molecular targets and may affect many pathophysiological processes resulting in improvement of cerebral ischemia outcomes. In this review, we summarize the main effects of cannabidiol in different animal models of cerebral ischemia and discuss some of its putative mechanisms of neuroprotection. Graphical Abstract Animal models (dpeaa)DE-He213 Cannabinoids (dpeaa)DE-He213 Cerebral blood flow (dpeaa)DE-He213 Impaired blood flow (dpeaa)DE-He213 Marijuana (dpeaa)DE-He213 Neuroprotection (dpeaa)DE-He213 de Mattos, Bianca Andretto (orcid)0000-0002-6325-1064 aut Kirchhoff, Frank (orcid)0000-0002-2324-2761 aut de Oliveira, Rúbia Maria Weffort (orcid)0000-0002-6181-1881 aut Enthalten in Revista Brasileira de farmacognosia Critiba : Soc. Brasileira de Farmacognosia, 1986 31(2021), 5 vom: Okt., Seite 579-591 (DE-627)730275531 (DE-600)2690840-2 1981-528X nnns volume:31 year:2021 number:5 month:10 pages:579-591 https://dx.doi.org/10.1007/s43450-021-00199-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 31 2021 5 10 579-591 |
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10.1007/s43450-021-00199-6 doi (DE-627)SPR045966397 (SPR)s43450-021-00199-6-e DE-627 ger DE-627 rakwb eng Meyer, Erika verfasserin (orcid)0000-0002-8425-6358 aut Neuroprotective Effects of Cannabidiol Under Cerebral Ischemic Conditions 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) under exclusive licence to Sociedade Brasileira de Farmacognosia 2021 Abstract The lack of blood flow during cerebral ischemic conditions results in multiple and intricate pathophysiological mechanisms including excitotoxicity, oxidative stress, neuroinflammation, white matter injury, and blood–brain barrier impairment. Despite numerous experimental studies that have been conducted in preclinical settings, current treatments for cerebral ischemia including mechanical and pharmacological therapies are limited, and often accompanied by significant side effects. Therefore, it is necessary to investigate new strategies for treating these conditions. Cannabidiol, the most abundant non-psychotomimetic compound obtained from Cannabis sativa L., Cannabaceae, is a pleiotropic compound acting in a variety of molecular targets and may affect many pathophysiological processes resulting in improvement of cerebral ischemia outcomes. In this review, we summarize the main effects of cannabidiol in different animal models of cerebral ischemia and discuss some of its putative mechanisms of neuroprotection. Graphical Abstract Animal models (dpeaa)DE-He213 Cannabinoids (dpeaa)DE-He213 Cerebral blood flow (dpeaa)DE-He213 Impaired blood flow (dpeaa)DE-He213 Marijuana (dpeaa)DE-He213 Neuroprotection (dpeaa)DE-He213 de Mattos, Bianca Andretto (orcid)0000-0002-6325-1064 aut Kirchhoff, Frank (orcid)0000-0002-2324-2761 aut de Oliveira, Rúbia Maria Weffort (orcid)0000-0002-6181-1881 aut Enthalten in Revista Brasileira de farmacognosia Critiba : Soc. Brasileira de Farmacognosia, 1986 31(2021), 5 vom: Okt., Seite 579-591 (DE-627)730275531 (DE-600)2690840-2 1981-528X nnns volume:31 year:2021 number:5 month:10 pages:579-591 https://dx.doi.org/10.1007/s43450-021-00199-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 31 2021 5 10 579-591 |
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10.1007/s43450-021-00199-6 doi (DE-627)SPR045966397 (SPR)s43450-021-00199-6-e DE-627 ger DE-627 rakwb eng Meyer, Erika verfasserin (orcid)0000-0002-8425-6358 aut Neuroprotective Effects of Cannabidiol Under Cerebral Ischemic Conditions 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) under exclusive licence to Sociedade Brasileira de Farmacognosia 2021 Abstract The lack of blood flow during cerebral ischemic conditions results in multiple and intricate pathophysiological mechanisms including excitotoxicity, oxidative stress, neuroinflammation, white matter injury, and blood–brain barrier impairment. Despite numerous experimental studies that have been conducted in preclinical settings, current treatments for cerebral ischemia including mechanical and pharmacological therapies are limited, and often accompanied by significant side effects. Therefore, it is necessary to investigate new strategies for treating these conditions. Cannabidiol, the most abundant non-psychotomimetic compound obtained from Cannabis sativa L., Cannabaceae, is a pleiotropic compound acting in a variety of molecular targets and may affect many pathophysiological processes resulting in improvement of cerebral ischemia outcomes. In this review, we summarize the main effects of cannabidiol in different animal models of cerebral ischemia and discuss some of its putative mechanisms of neuroprotection. Graphical Abstract Animal models (dpeaa)DE-He213 Cannabinoids (dpeaa)DE-He213 Cerebral blood flow (dpeaa)DE-He213 Impaired blood flow (dpeaa)DE-He213 Marijuana (dpeaa)DE-He213 Neuroprotection (dpeaa)DE-He213 de Mattos, Bianca Andretto (orcid)0000-0002-6325-1064 aut Kirchhoff, Frank (orcid)0000-0002-2324-2761 aut de Oliveira, Rúbia Maria Weffort (orcid)0000-0002-6181-1881 aut Enthalten in Revista Brasileira de farmacognosia Critiba : Soc. Brasileira de Farmacognosia, 1986 31(2021), 5 vom: Okt., Seite 579-591 (DE-627)730275531 (DE-600)2690840-2 1981-528X nnns volume:31 year:2021 number:5 month:10 pages:579-591 https://dx.doi.org/10.1007/s43450-021-00199-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 31 2021 5 10 579-591 |
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Enthalten in Revista Brasileira de farmacognosia 31(2021), 5 vom: Okt., Seite 579-591 volume:31 year:2021 number:5 month:10 pages:579-591 |
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Meyer, Erika @@aut@@ de Mattos, Bianca Andretto @@aut@@ Kirchhoff, Frank @@aut@@ de Oliveira, Rúbia Maria Weffort @@aut@@ |
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neuroprotective effects of cannabidiol under cerebral ischemic conditions |
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Neuroprotective Effects of Cannabidiol Under Cerebral Ischemic Conditions |
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Abstract The lack of blood flow during cerebral ischemic conditions results in multiple and intricate pathophysiological mechanisms including excitotoxicity, oxidative stress, neuroinflammation, white matter injury, and blood–brain barrier impairment. Despite numerous experimental studies that have been conducted in preclinical settings, current treatments for cerebral ischemia including mechanical and pharmacological therapies are limited, and often accompanied by significant side effects. Therefore, it is necessary to investigate new strategies for treating these conditions. Cannabidiol, the most abundant non-psychotomimetic compound obtained from Cannabis sativa L., Cannabaceae, is a pleiotropic compound acting in a variety of molecular targets and may affect many pathophysiological processes resulting in improvement of cerebral ischemia outcomes. In this review, we summarize the main effects of cannabidiol in different animal models of cerebral ischemia and discuss some of its putative mechanisms of neuroprotection. Graphical Abstract © The Author(s) under exclusive licence to Sociedade Brasileira de Farmacognosia 2021 |
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Abstract The lack of blood flow during cerebral ischemic conditions results in multiple and intricate pathophysiological mechanisms including excitotoxicity, oxidative stress, neuroinflammation, white matter injury, and blood–brain barrier impairment. Despite numerous experimental studies that have been conducted in preclinical settings, current treatments for cerebral ischemia including mechanical and pharmacological therapies are limited, and often accompanied by significant side effects. Therefore, it is necessary to investigate new strategies for treating these conditions. Cannabidiol, the most abundant non-psychotomimetic compound obtained from Cannabis sativa L., Cannabaceae, is a pleiotropic compound acting in a variety of molecular targets and may affect many pathophysiological processes resulting in improvement of cerebral ischemia outcomes. In this review, we summarize the main effects of cannabidiol in different animal models of cerebral ischemia and discuss some of its putative mechanisms of neuroprotection. Graphical Abstract © The Author(s) under exclusive licence to Sociedade Brasileira de Farmacognosia 2021 |
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Abstract The lack of blood flow during cerebral ischemic conditions results in multiple and intricate pathophysiological mechanisms including excitotoxicity, oxidative stress, neuroinflammation, white matter injury, and blood–brain barrier impairment. Despite numerous experimental studies that have been conducted in preclinical settings, current treatments for cerebral ischemia including mechanical and pharmacological therapies are limited, and often accompanied by significant side effects. Therefore, it is necessary to investigate new strategies for treating these conditions. Cannabidiol, the most abundant non-psychotomimetic compound obtained from Cannabis sativa L., Cannabaceae, is a pleiotropic compound acting in a variety of molecular targets and may affect many pathophysiological processes resulting in improvement of cerebral ischemia outcomes. In this review, we summarize the main effects of cannabidiol in different animal models of cerebral ischemia and discuss some of its putative mechanisms of neuroprotection. Graphical Abstract © The Author(s) under exclusive licence to Sociedade Brasileira de Farmacognosia 2021 |
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| title_short |
Neuroprotective Effects of Cannabidiol Under Cerebral Ischemic Conditions |
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https://dx.doi.org/10.1007/s43450-021-00199-6 |
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de Mattos, Bianca Andretto Kirchhoff, Frank de Oliveira, Rúbia Maria Weffort |
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10.1007/s43450-021-00199-6 |
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2024-07-03T19:27:26.355Z |
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| score |
7.4004374 |