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Ameliorative effects of 6‑gingerol in cerebral ischemia are mediated via the activation of antioxidant and anti‑inflammatory pathways

Focal ischemia occurs when an embolus or thrombus occludes an artery, causing the rapid obstruction of cerebral blood flow. Although stroke represents a main cause of disability and mortality in developing countries, therapeutic approaches available for this condition remain very limited. The aim of...

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Autores principales: Kongsui, Ratchaniporn, Jittiwat, Jinatta
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9996095/
https://www.ncbi.nlm.nih.gov/pubmed/36909941
http://dx.doi.org/10.3892/br.2023.1608
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author Kongsui, Ratchaniporn
Jittiwat, Jinatta
author_facet Kongsui, Ratchaniporn
Jittiwat, Jinatta
author_sort Kongsui, Ratchaniporn
collection PubMed
description Focal ischemia occurs when an embolus or thrombus occludes an artery, causing the rapid obstruction of cerebral blood flow. Although stroke represents a main cause of disability and mortality in developing countries, therapeutic approaches available for this condition remain very limited. The aim of the present study was to examine the effects of the phytochemical, 6-gingerol, on the brain infarct volume, neuronal loss and on the oxidative stress parameters, cyclooxygenase-2 (COX-2) and interleukin (IL)-6, in an animal model of focal ischemic stroke. Male Wistar rats, weighing 250-300 g, were divided into the following six groups: i) The control; ii) right middle cerebral artery occlusion (Rt.MCAO) + vehicle; iii) Rt.MCAO + piracetam; iv) Rt.MCAO + 6-gingerol (6-Gin) at 5 mg/kg body weight (BW); v) Rt.MCAO + 6-Gin at 10 mg/kg BW; and vi) the Rt.MCAO + 6-Gin at 20 mg/kg BW group. The rats in each group received the vehicle or piracetam or 6-gingerol intraperitoneally for 7 days following Rt.MCAO. The brain infarct volume, neuronal loss and alterations in antioxidant and anti-inflammatory levels were assessed in the cortex and hippocampus. The results revealed that the brain infarct volume, malondialdehyde level and the density ratio of COX-2 and IL-6 to β-actin were significantly decreased following treatment with 6-gingerol. In addition, neuronal density and superoxide dismutase activity in the cortex and hippocampus were increased. On the whole, the findings of the present study suggest that 6-gingerol exerts antioxidant and anti-inflammatory effects in vivo, which effectively ameliorate the brain damage induced by focal cerebral ischemic strok
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spelling pubmed-99960952023-03-10 Ameliorative effects of 6‑gingerol in cerebral ischemia are mediated via the activation of antioxidant and anti‑inflammatory pathways Kongsui, Ratchaniporn Jittiwat, Jinatta Biomed Rep Articles Focal ischemia occurs when an embolus or thrombus occludes an artery, causing the rapid obstruction of cerebral blood flow. Although stroke represents a main cause of disability and mortality in developing countries, therapeutic approaches available for this condition remain very limited. The aim of the present study was to examine the effects of the phytochemical, 6-gingerol, on the brain infarct volume, neuronal loss and on the oxidative stress parameters, cyclooxygenase-2 (COX-2) and interleukin (IL)-6, in an animal model of focal ischemic stroke. Male Wistar rats, weighing 250-300 g, were divided into the following six groups: i) The control; ii) right middle cerebral artery occlusion (Rt.MCAO) + vehicle; iii) Rt.MCAO + piracetam; iv) Rt.MCAO + 6-gingerol (6-Gin) at 5 mg/kg body weight (BW); v) Rt.MCAO + 6-Gin at 10 mg/kg BW; and vi) the Rt.MCAO + 6-Gin at 20 mg/kg BW group. The rats in each group received the vehicle or piracetam or 6-gingerol intraperitoneally for 7 days following Rt.MCAO. The brain infarct volume, neuronal loss and alterations in antioxidant and anti-inflammatory levels were assessed in the cortex and hippocampus. The results revealed that the brain infarct volume, malondialdehyde level and the density ratio of COX-2 and IL-6 to β-actin were significantly decreased following treatment with 6-gingerol. In addition, neuronal density and superoxide dismutase activity in the cortex and hippocampus were increased. On the whole, the findings of the present study suggest that 6-gingerol exerts antioxidant and anti-inflammatory effects in vivo, which effectively ameliorate the brain damage induced by focal cerebral ischemic strok D.A. Spandidos 2023-02-15 /pmc/articles/PMC9996095/ /pubmed/36909941 http://dx.doi.org/10.3892/br.2023.1608 Text en Copyright: © Kongsui et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Kongsui, Ratchaniporn
Jittiwat, Jinatta
Ameliorative effects of 6‑gingerol in cerebral ischemia are mediated via the activation of antioxidant and anti‑inflammatory pathways
title Ameliorative effects of 6‑gingerol in cerebral ischemia are mediated via the activation of antioxidant and anti‑inflammatory pathways
title_full Ameliorative effects of 6‑gingerol in cerebral ischemia are mediated via the activation of antioxidant and anti‑inflammatory pathways
title_fullStr Ameliorative effects of 6‑gingerol in cerebral ischemia are mediated via the activation of antioxidant and anti‑inflammatory pathways
title_full_unstemmed Ameliorative effects of 6‑gingerol in cerebral ischemia are mediated via the activation of antioxidant and anti‑inflammatory pathways
title_short Ameliorative effects of 6‑gingerol in cerebral ischemia are mediated via the activation of antioxidant and anti‑inflammatory pathways
title_sort ameliorative effects of 6‑gingerol in cerebral ischemia are mediated via the activation of antioxidant and anti‑inflammatory pathways
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9996095/
https://www.ncbi.nlm.nih.gov/pubmed/36909941
http://dx.doi.org/10.3892/br.2023.1608
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