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Endoplasmic Reticulum Stress and Autophagy Markers in Soleus Muscle Disuse-Induced Atrophy of Rats Treated with Fish Oil
Endoplasmic reticulum stress (ERS) and autophagy pathways are implicated in disuse muscle atrophy. The effects of high eicosapentaenoic (EPA) or high docosahexaenoic (DHA) fish oils on soleus muscle ERS and autophagy markers were investigated in a rat hindlimb suspension (HS) atrophy model. Adult Wi...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8308346/ https://www.ncbi.nlm.nih.gov/pubmed/34371808 http://dx.doi.org/10.3390/nu13072298 |
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author | Marzuca-Nassr, Gabriel Nasri Kuwabara, Wilson Mitsuo Tatagiba Vitzel, Kaio Fernando Murata, Gilson Masahiro Torres, Rosângela Pavan Mancini-Filho, Jorge Alba-Loureiro, Tatiana Carolina Curi, Rui |
author_facet | Marzuca-Nassr, Gabriel Nasri Kuwabara, Wilson Mitsuo Tatagiba Vitzel, Kaio Fernando Murata, Gilson Masahiro Torres, Rosângela Pavan Mancini-Filho, Jorge Alba-Loureiro, Tatiana Carolina Curi, Rui |
author_sort | Marzuca-Nassr, Gabriel Nasri |
collection | PubMed |
description | Endoplasmic reticulum stress (ERS) and autophagy pathways are implicated in disuse muscle atrophy. The effects of high eicosapentaenoic (EPA) or high docosahexaenoic (DHA) fish oils on soleus muscle ERS and autophagy markers were investigated in a rat hindlimb suspension (HS) atrophy model. Adult Wistar male rats received daily by gavage supplementation (0.3 mL per 100 g b.w.) of mineral oil or high EPA or high DHA fish oils (FOs) for two weeks. Afterward, the rats were subjected to HS and the respective treatments concomitantly for an additional two-week period. After four weeks, we evaluated ERS and autophagy markers in the soleus muscle. Results were analyzed using two-way analysis of variance (ANOVA) and Bonferroni post hoc test. Gastrocnemius muscle ω-6/ω-3 fatty acids (FAs) ratio was decreased by both FOs indicating the tissue incorporation of omega-3 fatty acids. HS altered (p < 0.05) the protein content (decreasing total p38 and BiP and increasing p-JNK2/total JNK2 ratio, and caspase 3) and gene expressions (decreasing BiP and increasing IRE1 and PERK) of ERS and autophagy (decreasing Beclin and increasing LC3 and ATG14) markers in soleus. Both FOs attenuated (p < 0.05) the increase in PERK and ATG14 expressions induced by HS. Thus, both FOs could potentially attenuate ERS and autophagy in skeletal muscles undergoing atrophy. |
format | Online Article Text |
id | pubmed-8308346 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-83083462021-07-25 Endoplasmic Reticulum Stress and Autophagy Markers in Soleus Muscle Disuse-Induced Atrophy of Rats Treated with Fish Oil Marzuca-Nassr, Gabriel Nasri Kuwabara, Wilson Mitsuo Tatagiba Vitzel, Kaio Fernando Murata, Gilson Masahiro Torres, Rosângela Pavan Mancini-Filho, Jorge Alba-Loureiro, Tatiana Carolina Curi, Rui Nutrients Article Endoplasmic reticulum stress (ERS) and autophagy pathways are implicated in disuse muscle atrophy. The effects of high eicosapentaenoic (EPA) or high docosahexaenoic (DHA) fish oils on soleus muscle ERS and autophagy markers were investigated in a rat hindlimb suspension (HS) atrophy model. Adult Wistar male rats received daily by gavage supplementation (0.3 mL per 100 g b.w.) of mineral oil or high EPA or high DHA fish oils (FOs) for two weeks. Afterward, the rats were subjected to HS and the respective treatments concomitantly for an additional two-week period. After four weeks, we evaluated ERS and autophagy markers in the soleus muscle. Results were analyzed using two-way analysis of variance (ANOVA) and Bonferroni post hoc test. Gastrocnemius muscle ω-6/ω-3 fatty acids (FAs) ratio was decreased by both FOs indicating the tissue incorporation of omega-3 fatty acids. HS altered (p < 0.05) the protein content (decreasing total p38 and BiP and increasing p-JNK2/total JNK2 ratio, and caspase 3) and gene expressions (decreasing BiP and increasing IRE1 and PERK) of ERS and autophagy (decreasing Beclin and increasing LC3 and ATG14) markers in soleus. Both FOs attenuated (p < 0.05) the increase in PERK and ATG14 expressions induced by HS. Thus, both FOs could potentially attenuate ERS and autophagy in skeletal muscles undergoing atrophy. MDPI 2021-07-03 /pmc/articles/PMC8308346/ /pubmed/34371808 http://dx.doi.org/10.3390/nu13072298 Text en © 2021 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 Marzuca-Nassr, Gabriel Nasri Kuwabara, Wilson Mitsuo Tatagiba Vitzel, Kaio Fernando Murata, Gilson Masahiro Torres, Rosângela Pavan Mancini-Filho, Jorge Alba-Loureiro, Tatiana Carolina Curi, Rui Endoplasmic Reticulum Stress and Autophagy Markers in Soleus Muscle Disuse-Induced Atrophy of Rats Treated with Fish Oil |
title | Endoplasmic Reticulum Stress and Autophagy Markers in Soleus Muscle Disuse-Induced Atrophy of Rats Treated with Fish Oil |
title_full | Endoplasmic Reticulum Stress and Autophagy Markers in Soleus Muscle Disuse-Induced Atrophy of Rats Treated with Fish Oil |
title_fullStr | Endoplasmic Reticulum Stress and Autophagy Markers in Soleus Muscle Disuse-Induced Atrophy of Rats Treated with Fish Oil |
title_full_unstemmed | Endoplasmic Reticulum Stress and Autophagy Markers in Soleus Muscle Disuse-Induced Atrophy of Rats Treated with Fish Oil |
title_short | Endoplasmic Reticulum Stress and Autophagy Markers in Soleus Muscle Disuse-Induced Atrophy of Rats Treated with Fish Oil |
title_sort | endoplasmic reticulum stress and autophagy markers in soleus muscle disuse-induced atrophy of rats treated with fish oil |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8308346/ https://www.ncbi.nlm.nih.gov/pubmed/34371808 http://dx.doi.org/10.3390/nu13072298 |
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