The Hepatoprotective mechanisms of 17β-estradiol after traumatic brain injury in male rats: Classical and non-classical estrogen receptors
Protective effects of estrogen (E2) on traumatic brain injury (TBI) have been determined. In this study, the hepatoprotective effects of E2 after TBI through its receptors and oxidative stress regulation have been evaluated. Diffuse TBI induced by the Marmarou method in male rats. G15, PHTPP, MPP, a...
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| Format: | Article |
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Elsevier
2021-04-01
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| Series: | Ecotoxicology and Environmental Safety |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651321000981 |
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| author | Sedigheh Amiresmaili Nader Shahrokhi Mohammad Khaksari Gholamreza AsadiKaram Mohammad Reza Aflatoonian Sara Shirazpour Ladan Amirkhosravi Abbas Mortazaeizadeh |
| author_facet | Sedigheh Amiresmaili Nader Shahrokhi Mohammad Khaksari Gholamreza AsadiKaram Mohammad Reza Aflatoonian Sara Shirazpour Ladan Amirkhosravi Abbas Mortazaeizadeh |
| author_sort | Sedigheh Amiresmaili |
| collection | DOAJ |
| description | Protective effects of estrogen (E2) on traumatic brain injury (TBI) have been determined. In this study, the hepatoprotective effects of E2 after TBI through its receptors and oxidative stress regulation have been evaluated. Diffuse TBI induced by the Marmarou method in male rats. G15, PHTPP, MPP, and ICI182–780 as selective antagonists of E2 were injected before TBI. The results indicated that TBI induces a significant increase in liver enzymes [Alkaline phosphatase (ALP), Aspartate aminotransferase (AST), Alanine aminotransferase (ALT), Glutamyl transferase (GGT)], and oxidants levels [Malondialdehyde (MDA), Nitric oxide (NO)] and decreases in antioxidant biomarkers [Glutathione peroxidase (GPx) and Superoxide dismutase (SOD)] in the brain and liver, and plasma. We also found that E2 significantly preserved levels of these biomarkers and enzymatic activity. All antagonists inhibited the effects of E2 on increasing SOD and GPx. Also, the effects of E2 on brain MDA levels were inhibited by all antagonists, but in the liver, only ICI + G15 + E2 + TBI group was affected. The impacts of E2 on brain and liver and plasma NO levels were inhibited by all antagonists. The current findings demonstrated that E2 probably improved liver injury after TBI by modulating oxidative stress. Also, both classic (ERβ, ERα) and non-classic [G protein-coupled estrogen receptor (GPER)] receptors are affected in the protective effects of E2. |
| first_indexed | 2024-12-24T10:04:41Z |
| format | Article |
| id | doaj.art-bbf7fed152ec46ba8a9e26ebf852a3b4 |
| institution | Directory Open Access Journal |
| issn | 0147-6513 |
| language | English |
| last_indexed | 2024-12-24T10:04:41Z |
| publishDate | 2021-04-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| spelling | doaj.art-bbf7fed152ec46ba8a9e26ebf852a3b42022-12-21T17:00:53ZengElsevierEcotoxicology and Environmental Safety0147-65132021-04-01213111987The Hepatoprotective mechanisms of 17β-estradiol after traumatic brain injury in male rats: Classical and non-classical estrogen receptorsSedigheh Amiresmaili0Nader Shahrokhi1Mohammad Khaksari2Gholamreza AsadiKaram3Mohammad Reza Aflatoonian4Sara Shirazpour5Ladan Amirkhosravi6Abbas Mortazaeizadeh7Department of Physiology, Bam University of Medical Sciences, Bam, Iran; Physiology Research Center, Institute of Basic and Clinical Physiology Science, Kerman University of Medical Sciences, Kerman, IranNeuroscience Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran; Correspondence to: Physiology and Neuroscience Research Centers, Kerman University of Medical Sciences, Kerman, Iran.Endocrinology and Metabolism Research Center, Institute of Basic and Clinical Physiology Science, Kerman University of Medical Sciences, Kerman, IranPhysiology Research Center, Institute of Basic and Clinical Physiology Science, Kerman University of Medical Sciences, Kerman, IranNano BioElectrochemistry Research Center, Bam University of Medical Sciences, Bam, IranNeuroscience Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, IranEndocrinology and Metabolism Research Center, Institute of Basic and Clinical Physiology Science, Kerman University of Medical Sciences, Kerman, IranResearcher, Pathology and Stem Cells Research Center, Kerman University of Medical Sciences, Kerman, IranProtective effects of estrogen (E2) on traumatic brain injury (TBI) have been determined. In this study, the hepatoprotective effects of E2 after TBI through its receptors and oxidative stress regulation have been evaluated. Diffuse TBI induced by the Marmarou method in male rats. G15, PHTPP, MPP, and ICI182–780 as selective antagonists of E2 were injected before TBI. The results indicated that TBI induces a significant increase in liver enzymes [Alkaline phosphatase (ALP), Aspartate aminotransferase (AST), Alanine aminotransferase (ALT), Glutamyl transferase (GGT)], and oxidants levels [Malondialdehyde (MDA), Nitric oxide (NO)] and decreases in antioxidant biomarkers [Glutathione peroxidase (GPx) and Superoxide dismutase (SOD)] in the brain and liver, and plasma. We also found that E2 significantly preserved levels of these biomarkers and enzymatic activity. All antagonists inhibited the effects of E2 on increasing SOD and GPx. Also, the effects of E2 on brain MDA levels were inhibited by all antagonists, but in the liver, only ICI + G15 + E2 + TBI group was affected. The impacts of E2 on brain and liver and plasma NO levels were inhibited by all antagonists. The current findings demonstrated that E2 probably improved liver injury after TBI by modulating oxidative stress. Also, both classic (ERβ, ERα) and non-classic [G protein-coupled estrogen receptor (GPER)] receptors are affected in the protective effects of E2.http://www.sciencedirect.com/science/article/pii/S0147651321000981Traumatic brain injury17β-estradiolHepatoprotectionOxidative stressEstrogen receptors |
| spellingShingle | Sedigheh Amiresmaili Nader Shahrokhi Mohammad Khaksari Gholamreza AsadiKaram Mohammad Reza Aflatoonian Sara Shirazpour Ladan Amirkhosravi Abbas Mortazaeizadeh The Hepatoprotective mechanisms of 17β-estradiol after traumatic brain injury in male rats: Classical and non-classical estrogen receptors Ecotoxicology and Environmental Safety Traumatic brain injury 17β-estradiol Hepatoprotection Oxidative stress Estrogen receptors |
| title | The Hepatoprotective mechanisms of 17β-estradiol after traumatic brain injury in male rats: Classical and non-classical estrogen receptors |
| title_full | The Hepatoprotective mechanisms of 17β-estradiol after traumatic brain injury in male rats: Classical and non-classical estrogen receptors |
| title_fullStr | The Hepatoprotective mechanisms of 17β-estradiol after traumatic brain injury in male rats: Classical and non-classical estrogen receptors |
| title_full_unstemmed | The Hepatoprotective mechanisms of 17β-estradiol after traumatic brain injury in male rats: Classical and non-classical estrogen receptors |
| title_short | The Hepatoprotective mechanisms of 17β-estradiol after traumatic brain injury in male rats: Classical and non-classical estrogen receptors |
| title_sort | hepatoprotective mechanisms of 17β estradiol after traumatic brain injury in male rats classical and non classical estrogen receptors |
| topic | Traumatic brain injury 17β-estradiol Hepatoprotection Oxidative stress Estrogen receptors |
| url | http://www.sciencedirect.com/science/article/pii/S0147651321000981 |
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