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Insamgobonhwan Protects Neuronal Cells from Lipid ROS and Improves Deficient Cognitive Function

Iron is an essential element in the central nervous system that is involved in many of its important biological processes, such as oxygen transportation, myelin production, and neurotransmitter synthesis. Previous studies have observed the selective accumulation of iron in Aβ aggregates and neurofib...

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Autores principales: Yang, Ji Hye, Nguyen, Cong Duc, Lee, Gihyun, Na, Chang-Su
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8868228/
https://www.ncbi.nlm.nih.gov/pubmed/35204177
http://dx.doi.org/10.3390/antiox11020295
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author Yang, Ji Hye
Nguyen, Cong Duc
Lee, Gihyun
Na, Chang-Su
author_facet Yang, Ji Hye
Nguyen, Cong Duc
Lee, Gihyun
Na, Chang-Su
author_sort Yang, Ji Hye
collection PubMed
description Iron is an essential element in the central nervous system that is involved in many of its important biological processes, such as oxygen transportation, myelin production, and neurotransmitter synthesis. Previous studies have observed the selective accumulation of iron in Aβ aggregates and neurofibrillary tangles in the brains of patients with Alzheimer’s disease, and excess of this accumulation is associated with accelerated cognitive decline in Alzheimer’s patients. Emerging evidence suggests that ferroptosis, cell death due to iron accumulation, is a potential therapeutic target for treating Alzheimer’s disease. Insamgobonhwan (GBH) is a well-regarded traditional medicine from Donguibogam that possess antioxidant properties and has been suggested to slow the aging process. However, the neuroprotective role of GBH against lipid peroxidation-induced ferroptosis and its positive cognitive effects remain unexplored. Here, we investigated the ability of GBH to protect against RSL3-induced ferroptosis in vitro and to suppress amyloid-β-induced cognitive impairment in vivo. First, we treated HT22 cells with RSL3 to induce ferroptosis, which is an inhibitor of glutathione peroxidase 4 (GPX4) and induces lethal lipid hydroperoxide accumulation, reactive oxygen species (ROS) production, and ferroptotic cell death. GBH treatment inhibited cell death and lipid peroxidation, which were increased by RSL3 administration. In addition, GBH restored the expression of ferroptosis marker proteins, such as GPX4, HO-1 and COX-2, which were altered by RSL3. Next, we examined whether the protective ability of GBH in cells was reproduced in animals. We concluded that GBH treatment inhibited Aβ-induced lipid peroxidation and improved Aβ-induced cognitive impairment in mice.
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spelling pubmed-88682282022-02-25 Insamgobonhwan Protects Neuronal Cells from Lipid ROS and Improves Deficient Cognitive Function Yang, Ji Hye Nguyen, Cong Duc Lee, Gihyun Na, Chang-Su Antioxidants (Basel) Article Iron is an essential element in the central nervous system that is involved in many of its important biological processes, such as oxygen transportation, myelin production, and neurotransmitter synthesis. Previous studies have observed the selective accumulation of iron in Aβ aggregates and neurofibrillary tangles in the brains of patients with Alzheimer’s disease, and excess of this accumulation is associated with accelerated cognitive decline in Alzheimer’s patients. Emerging evidence suggests that ferroptosis, cell death due to iron accumulation, is a potential therapeutic target for treating Alzheimer’s disease. Insamgobonhwan (GBH) is a well-regarded traditional medicine from Donguibogam that possess antioxidant properties and has been suggested to slow the aging process. However, the neuroprotective role of GBH against lipid peroxidation-induced ferroptosis and its positive cognitive effects remain unexplored. Here, we investigated the ability of GBH to protect against RSL3-induced ferroptosis in vitro and to suppress amyloid-β-induced cognitive impairment in vivo. First, we treated HT22 cells with RSL3 to induce ferroptosis, which is an inhibitor of glutathione peroxidase 4 (GPX4) and induces lethal lipid hydroperoxide accumulation, reactive oxygen species (ROS) production, and ferroptotic cell death. GBH treatment inhibited cell death and lipid peroxidation, which were increased by RSL3 administration. In addition, GBH restored the expression of ferroptosis marker proteins, such as GPX4, HO-1 and COX-2, which were altered by RSL3. Next, we examined whether the protective ability of GBH in cells was reproduced in animals. We concluded that GBH treatment inhibited Aβ-induced lipid peroxidation and improved Aβ-induced cognitive impairment in mice. MDPI 2022-01-31 /pmc/articles/PMC8868228/ /pubmed/35204177 http://dx.doi.org/10.3390/antiox11020295 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Yang, Ji Hye
Nguyen, Cong Duc
Lee, Gihyun
Na, Chang-Su
Insamgobonhwan Protects Neuronal Cells from Lipid ROS and Improves Deficient Cognitive Function
title Insamgobonhwan Protects Neuronal Cells from Lipid ROS and Improves Deficient Cognitive Function
title_full Insamgobonhwan Protects Neuronal Cells from Lipid ROS and Improves Deficient Cognitive Function
title_fullStr Insamgobonhwan Protects Neuronal Cells from Lipid ROS and Improves Deficient Cognitive Function
title_full_unstemmed Insamgobonhwan Protects Neuronal Cells from Lipid ROS and Improves Deficient Cognitive Function
title_short Insamgobonhwan Protects Neuronal Cells from Lipid ROS and Improves Deficient Cognitive Function
title_sort insamgobonhwan protects neuronal cells from lipid ros and improves deficient cognitive function
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8868228/
https://www.ncbi.nlm.nih.gov/pubmed/35204177
http://dx.doi.org/10.3390/antiox11020295
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