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Curcumin ameliorates chronic obstructive pulmonary disease by modulating autophagy and endoplasmic reticulum stress through regulation of SIRT1 in a rat model
OBJECTIVES: The ability of curcumin to activate SIRT1 and thereby promote autophagy and inhibit endoplasmic reticulum stress (ERS) in chronic obstructive pulmonary disease (COPD) remains unclear. We investigated the relationship between curcumin and SIRT1 activation in relation to autophagy and ERS...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE Publications
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6833429/ https://www.ncbi.nlm.nih.gov/pubmed/31510839 http://dx.doi.org/10.1177/0300060519869459 |
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author | Tang, Feng Ling, Chunhua |
author_facet | Tang, Feng Ling, Chunhua |
author_sort | Tang, Feng |
collection | PubMed |
description | OBJECTIVES: The ability of curcumin to activate SIRT1 and thereby promote autophagy and inhibit endoplasmic reticulum stress (ERS) in chronic obstructive pulmonary disease (COPD) remains unclear. We investigated the relationship between curcumin and SIRT1 activation in relation to autophagy and ERS in COPD. METHODS: We developed a rat COPD model by cigarette smoke exposure, and divided the rats into control, COPD, COPD + low-dose curcumin (50 mg/kg), COPD + medium-dose curcumin (100 mg/kg), COPD + high-dose curcumin (150 mg/kg), and COPD + high-dose curcumin + sirtinol (2 mM, 30 μL/kg) groups. Apoptosis was detected by TUNEL assay. SIRT1 gene and protein expression, and protein expression of autophagy-related genes LC3-I, LC3-II, and Beclin1, and ERS-related genes CHOP and GRP78 were measured by reverse transcription-polymerase chain reaction and western blot. RESULTS: SIRT1, LC3-I, LC3-II, and Beclin1 expression were significantly decreased and CHOP and GRP78 were enhanced in COPD compared with control rats. Curcumin increased the expression of SIRT1, LC3-I, LC3-II, and Beclin1 and decreased the expression of CHOP and GRP78 in COPD rats. The alleviating effects of curcumin on COPD in the SIRT1-inhibition group were reversed by suppressing LC3-I, LC3-II, and Beclin1 and increasing CHOP and GRP78. CONCLUSION: Curcumin might alleviate COPD by promoting autophagy and inhibiting ERS through SIRT1 activation. |
format | Online Article Text |
id | pubmed-6833429 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-68334292019-11-13 Curcumin ameliorates chronic obstructive pulmonary disease by modulating autophagy and endoplasmic reticulum stress through regulation of SIRT1 in a rat model Tang, Feng Ling, Chunhua J Int Med Res Clinical Research Reports OBJECTIVES: The ability of curcumin to activate SIRT1 and thereby promote autophagy and inhibit endoplasmic reticulum stress (ERS) in chronic obstructive pulmonary disease (COPD) remains unclear. We investigated the relationship between curcumin and SIRT1 activation in relation to autophagy and ERS in COPD. METHODS: We developed a rat COPD model by cigarette smoke exposure, and divided the rats into control, COPD, COPD + low-dose curcumin (50 mg/kg), COPD + medium-dose curcumin (100 mg/kg), COPD + high-dose curcumin (150 mg/kg), and COPD + high-dose curcumin + sirtinol (2 mM, 30 μL/kg) groups. Apoptosis was detected by TUNEL assay. SIRT1 gene and protein expression, and protein expression of autophagy-related genes LC3-I, LC3-II, and Beclin1, and ERS-related genes CHOP and GRP78 were measured by reverse transcription-polymerase chain reaction and western blot. RESULTS: SIRT1, LC3-I, LC3-II, and Beclin1 expression were significantly decreased and CHOP and GRP78 were enhanced in COPD compared with control rats. Curcumin increased the expression of SIRT1, LC3-I, LC3-II, and Beclin1 and decreased the expression of CHOP and GRP78 in COPD rats. The alleviating effects of curcumin on COPD in the SIRT1-inhibition group were reversed by suppressing LC3-I, LC3-II, and Beclin1 and increasing CHOP and GRP78. CONCLUSION: Curcumin might alleviate COPD by promoting autophagy and inhibiting ERS through SIRT1 activation. SAGE Publications 2019-09-12 2019-10 /pmc/articles/PMC6833429/ /pubmed/31510839 http://dx.doi.org/10.1177/0300060519869459 Text en © The Author(s) 2019 http://creativecommons.org/licenses/by-nc/4.0/ Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Clinical Research Reports Tang, Feng Ling, Chunhua Curcumin ameliorates chronic obstructive pulmonary disease by modulating autophagy and endoplasmic reticulum stress through regulation of SIRT1 in a rat model |
title | Curcumin ameliorates chronic obstructive pulmonary disease by modulating autophagy and endoplasmic reticulum stress through regulation of SIRT1 in a rat model |
title_full | Curcumin ameliorates chronic obstructive pulmonary disease by modulating autophagy and endoplasmic reticulum stress through regulation of SIRT1 in a rat model |
title_fullStr | Curcumin ameliorates chronic obstructive pulmonary disease by modulating autophagy and endoplasmic reticulum stress through regulation of SIRT1 in a rat model |
title_full_unstemmed | Curcumin ameliorates chronic obstructive pulmonary disease by modulating autophagy and endoplasmic reticulum stress through regulation of SIRT1 in a rat model |
title_short | Curcumin ameliorates chronic obstructive pulmonary disease by modulating autophagy and endoplasmic reticulum stress through regulation of SIRT1 in a rat model |
title_sort | curcumin ameliorates chronic obstructive pulmonary disease by modulating autophagy and endoplasmic reticulum stress through regulation of sirt1 in a rat model |
topic | Clinical Research Reports |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6833429/ https://www.ncbi.nlm.nih.gov/pubmed/31510839 http://dx.doi.org/10.1177/0300060519869459 |
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