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Diphlorethohydroxycarmalol Derived from Ishige okamurae Improves Behavioral and Physiological Responses of Muscle Atrophy Induced by Dexamethasone in an In-Vivo Model
Muscle atrophy refers to the loss of skeletal muscle mass, myofiber size, and related physical functions such as walking speed or grip strength caused by aging or a lack of physical activity due to injury or illness and can also be attributed to excessive exposure to corticosteroids. Ishige okamurae...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9026865/ https://www.ncbi.nlm.nih.gov/pubmed/35456553 http://dx.doi.org/10.3390/pharmaceutics14040719 |
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author | Ryu, Bomi Oh, Seyeon Yang, Hye-Won Sosorburam, Batsukh Chung, Dong-Min Seo, Minyoung Park, Shin-Jae Byun, Kyunghee Jeon, You-Jin |
author_facet | Ryu, Bomi Oh, Seyeon Yang, Hye-Won Sosorburam, Batsukh Chung, Dong-Min Seo, Minyoung Park, Shin-Jae Byun, Kyunghee Jeon, You-Jin |
author_sort | Ryu, Bomi |
collection | PubMed |
description | Muscle atrophy refers to the loss of skeletal muscle mass, myofiber size, and related physical functions such as walking speed or grip strength caused by aging or a lack of physical activity due to injury or illness and can also be attributed to excessive exposure to corticosteroids. Ishige okamurae (IO) and its active component, diphlorethohydroxycarmalol (DPHC), have been known to improve glucose homeostasis by controlling the contraction of skeletal muscles. Based on this idea, we hypothesized that the effects of DPHC and IO extract on muscle metabolism are associated with their role in improving muscle physical function. This study assessed the effects of DPHC or IO extract on muscle behavioral responses with their metabolic properties in muscle atrophy induced by glucocorticoids and dexamethasone (DEX) in vivo. In addition to the improvement in muscle behavioral response by DPHC or IO extract, the loss of muscle fiber and the related metabolic properties by DEX exposure in the gastrocnemius and soleus of calf muscle was prevented. These findings suggest that IO extract and its active component DPHC can potentially prevent muscle atrophy caused by exposure to corticosteroids and could be used to treat reverse skeletal atrophy. |
format | Online Article Text |
id | pubmed-9026865 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-90268652022-04-23 Diphlorethohydroxycarmalol Derived from Ishige okamurae Improves Behavioral and Physiological Responses of Muscle Atrophy Induced by Dexamethasone in an In-Vivo Model Ryu, Bomi Oh, Seyeon Yang, Hye-Won Sosorburam, Batsukh Chung, Dong-Min Seo, Minyoung Park, Shin-Jae Byun, Kyunghee Jeon, You-Jin Pharmaceutics Article Muscle atrophy refers to the loss of skeletal muscle mass, myofiber size, and related physical functions such as walking speed or grip strength caused by aging or a lack of physical activity due to injury or illness and can also be attributed to excessive exposure to corticosteroids. Ishige okamurae (IO) and its active component, diphlorethohydroxycarmalol (DPHC), have been known to improve glucose homeostasis by controlling the contraction of skeletal muscles. Based on this idea, we hypothesized that the effects of DPHC and IO extract on muscle metabolism are associated with their role in improving muscle physical function. This study assessed the effects of DPHC or IO extract on muscle behavioral responses with their metabolic properties in muscle atrophy induced by glucocorticoids and dexamethasone (DEX) in vivo. In addition to the improvement in muscle behavioral response by DPHC or IO extract, the loss of muscle fiber and the related metabolic properties by DEX exposure in the gastrocnemius and soleus of calf muscle was prevented. These findings suggest that IO extract and its active component DPHC can potentially prevent muscle atrophy caused by exposure to corticosteroids and could be used to treat reverse skeletal atrophy. MDPI 2022-03-27 /pmc/articles/PMC9026865/ /pubmed/35456553 http://dx.doi.org/10.3390/pharmaceutics14040719 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 Ryu, Bomi Oh, Seyeon Yang, Hye-Won Sosorburam, Batsukh Chung, Dong-Min Seo, Minyoung Park, Shin-Jae Byun, Kyunghee Jeon, You-Jin Diphlorethohydroxycarmalol Derived from Ishige okamurae Improves Behavioral and Physiological Responses of Muscle Atrophy Induced by Dexamethasone in an In-Vivo Model |
title | Diphlorethohydroxycarmalol Derived from Ishige okamurae Improves Behavioral and Physiological Responses of Muscle Atrophy Induced by Dexamethasone in an In-Vivo Model |
title_full | Diphlorethohydroxycarmalol Derived from Ishige okamurae Improves Behavioral and Physiological Responses of Muscle Atrophy Induced by Dexamethasone in an In-Vivo Model |
title_fullStr | Diphlorethohydroxycarmalol Derived from Ishige okamurae Improves Behavioral and Physiological Responses of Muscle Atrophy Induced by Dexamethasone in an In-Vivo Model |
title_full_unstemmed | Diphlorethohydroxycarmalol Derived from Ishige okamurae Improves Behavioral and Physiological Responses of Muscle Atrophy Induced by Dexamethasone in an In-Vivo Model |
title_short | Diphlorethohydroxycarmalol Derived from Ishige okamurae Improves Behavioral and Physiological Responses of Muscle Atrophy Induced by Dexamethasone in an In-Vivo Model |
title_sort | diphlorethohydroxycarmalol derived from ishige okamurae improves behavioral and physiological responses of muscle atrophy induced by dexamethasone in an in-vivo model |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9026865/ https://www.ncbi.nlm.nih.gov/pubmed/35456553 http://dx.doi.org/10.3390/pharmaceutics14040719 |
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