Grape-Leaf Extract Attenuates Alcohol-Induced Liver Injury via Interference with NF-κB Signaling Pathway
Grape (<i>Vitis vinifera</i>) leaf extracts (GLEs) are known to be rich in phenolic compounds that exert potent antioxidant effects. Given the vulnerability of the liver to oxidative damage, antioxidants have been proposed as therapeutic agents and coadjuvant drugs to ameliorate liver pa...
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2020-04-01
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author | Yhiya Amen Asmaa E. Sherif Noha M. Shawky Rehab S. Abdelrahman Michael Wink Mansour Sobeh |
author_facet | Yhiya Amen Asmaa E. Sherif Noha M. Shawky Rehab S. Abdelrahman Michael Wink Mansour Sobeh |
author_sort | Yhiya Amen |
collection | DOAJ |
description | Grape (<i>Vitis vinifera</i>) leaf extracts (GLEs) are known to be rich in phenolic compounds that exert potent antioxidant effects. Given the vulnerability of the liver to oxidative damage, antioxidants have been proposed as therapeutic agents and coadjuvant drugs to ameliorate liver pathologies. The current study was designed to characterize secondary metabolites and investigate the hepatoprotective effects of GLE and its underlying mechanisms. The secondary metabolites were profiled using HPLC–PDA–ESI-MS, and forty-five compounds were tentatively identified. In experimental in vivo design, liver injury was induced by oral administration of high doses of ethanol (EtOH) for 12 days to male Sprague Dawley rats that were split into five different groups. Blood samples and livers were then collected, and used for various biochemical, immunohistochemical, and histopathological analyses. Results showed that GLE-attenuated liver injury and promoted marked hepatic antioxidant effects, in addition to suppressing the increased heat-shock protein-70 expression. Moreover, GLE suppressed EtOH-induced expression of nuclear factor-κB (NF-κB) p65 subunit and proinflammatory cytokine tumor necrosis factor-α. Caspase-3 and survivin were enhanced by EtOH intake and suppressed by GLE intake. Finally, EtOH-induced histopathological changes in liver sections were markedly normalized by GLE. In conclusion, our results suggested that GLE interferes with NF-κB signaling and induces antioxidant effects, which both play a role in attenuating apoptosis and associated liver injury in a model of EtOH-induced liver damage in rats. |
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spelling | doaj.art-60ac203b4dbb4c99bcb728451edd9ac52023-11-19T20:48:53ZengMDPI AGBiomolecules2218-273X2020-04-0110455810.3390/biom10040558Grape-Leaf Extract Attenuates Alcohol-Induced Liver Injury via Interference with NF-κB Signaling PathwayYhiya Amen0Asmaa E. Sherif1Noha M. Shawky2Rehab S. Abdelrahman3Michael Wink4Mansour Sobeh5Department of Pharmacognosy, Faculty of Pharmacy, Mansoura University, Mansoura 35516, EgyptDepartment of Pharmacognosy, Faculty of Pharmacy, Mansoura University, Mansoura 35516, EgyptDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Mansoura University, Mansoura 35516, EgyptDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Mansoura University, Mansoura 35516, EgyptInstitute of Pharmacy and Molecular Biotechnology, Heidelberg University, Im Neuenheimer Feld 364, 69120 Heidelberg, GermanyInstitute of Pharmacy and Molecular Biotechnology, Heidelberg University, Im Neuenheimer Feld 364, 69120 Heidelberg, GermanyGrape (<i>Vitis vinifera</i>) leaf extracts (GLEs) are known to be rich in phenolic compounds that exert potent antioxidant effects. Given the vulnerability of the liver to oxidative damage, antioxidants have been proposed as therapeutic agents and coadjuvant drugs to ameliorate liver pathologies. The current study was designed to characterize secondary metabolites and investigate the hepatoprotective effects of GLE and its underlying mechanisms. The secondary metabolites were profiled using HPLC–PDA–ESI-MS, and forty-five compounds were tentatively identified. In experimental in vivo design, liver injury was induced by oral administration of high doses of ethanol (EtOH) for 12 days to male Sprague Dawley rats that were split into five different groups. Blood samples and livers were then collected, and used for various biochemical, immunohistochemical, and histopathological analyses. Results showed that GLE-attenuated liver injury and promoted marked hepatic antioxidant effects, in addition to suppressing the increased heat-shock protein-70 expression. Moreover, GLE suppressed EtOH-induced expression of nuclear factor-κB (NF-κB) p65 subunit and proinflammatory cytokine tumor necrosis factor-α. Caspase-3 and survivin were enhanced by EtOH intake and suppressed by GLE intake. Finally, EtOH-induced histopathological changes in liver sections were markedly normalized by GLE. In conclusion, our results suggested that GLE interferes with NF-κB signaling and induces antioxidant effects, which both play a role in attenuating apoptosis and associated liver injury in a model of EtOH-induced liver damage in rats.https://www.mdpi.com/2218-273X/10/4/558grape-leaf extractoxidative stressNF-κBapoptosisLC-MSliver injury |
spellingShingle | Yhiya Amen Asmaa E. Sherif Noha M. Shawky Rehab S. Abdelrahman Michael Wink Mansour Sobeh Grape-Leaf Extract Attenuates Alcohol-Induced Liver Injury via Interference with NF-κB Signaling Pathway Biomolecules grape-leaf extract oxidative stress NF-κB apoptosis LC-MS liver injury |
title | Grape-Leaf Extract Attenuates Alcohol-Induced Liver Injury via Interference with NF-κB Signaling Pathway |
title_full | Grape-Leaf Extract Attenuates Alcohol-Induced Liver Injury via Interference with NF-κB Signaling Pathway |
title_fullStr | Grape-Leaf Extract Attenuates Alcohol-Induced Liver Injury via Interference with NF-κB Signaling Pathway |
title_full_unstemmed | Grape-Leaf Extract Attenuates Alcohol-Induced Liver Injury via Interference with NF-κB Signaling Pathway |
title_short | Grape-Leaf Extract Attenuates Alcohol-Induced Liver Injury via Interference with NF-κB Signaling Pathway |
title_sort | grape leaf extract attenuates alcohol induced liver injury via interference with nf κb signaling pathway |
topic | grape-leaf extract oxidative stress NF-κB apoptosis LC-MS liver injury |
url | https://www.mdpi.com/2218-273X/10/4/558 |
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