Adiponectin Protects Obese Rats from Aggravated Acute Lung Injury via Suppression of Endoplasmic Reticulum Stress

Ke Wei,1 Jie Luo,1 Jun Cao,1 Lihua Peng,1 Li Ren,1 Fan Zhang2 1Department of Anesthesiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, People’s Republic of China; 2Department of Anesthesiology, Jianyang People’s Hospital, Jianyang, Sichuan...

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Autores principales:	Wei K, Luo J, Cao J, Peng L, Ren L, Zhang F
Formato:	article
Lenguaje:	EN
Publicado:	Dove Medical Press 2020
Materias:	adiponectin endoplasmic reticulum stress obesity lung injury Specialties of internal medicine RC581-951
Acceso en línea:	https://doaj.org/article/4fa3433b35f24508a88178286455f991
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spelling	oai:doaj.org-article:4fa3433b35f24508a88178286455f9912021-12-02T12:48:12ZAdiponectin Protects Obese Rats from Aggravated Acute Lung Injury via Suppression of Endoplasmic Reticulum Stress1178-7007https://doaj.org/article/4fa3433b35f24508a88178286455f9912020-11-01T00:00:00Zhttps://www.dovepress.com/adiponectin-protects-obese-rats-from-aggravated-acute-lung-injury-via--peer-reviewed-article-DMSOhttps://doaj.org/toc/1178-7007Ke Wei,1 Jie Luo,1 Jun Cao,1 Lihua Peng,1 Li Ren,1 Fan Zhang2 1Department of Anesthesiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, People’s Republic of China; 2Department of Anesthesiology, Jianyang People’s Hospital, Jianyang, Sichuan 641400, People’s Republic of ChinaCorrespondence: Ke WeiDepartment of Anesthesiology, The First Affiliated Hospital of Chongqing Medical University, 1# Youyi Road, Yuzhong District, Chongqing, People’s Republic of ChinaTel +86 23 89011069Fax +86 23 89011062Email wk202448@hospital-cqmu.comIntroduction: Endoplasmic reticulum (ER) stress seems to mediate the obesity-induced susceptibility to acute lung injury (ALI). The present study was designed to evaluate the role of ER stress in adiponectin (APN)-induced lung protection in an obese rat model treated with lipopolysaccharide (LPS).Methods: Four-week-old male Sprague-Dawley rats fed either a normal chow diet or a high-fat diet for 12 weeks were randomly assigned to one of the following groups: lean rats, diet-induced obesity rats, lean rats with ALI, obese rats with ALI, obese rats pretreated with 4-phenylbutyric acid (4-PBA) before ALI or obese rats pretreated with APN before ALI. At 24 h after instillation of LPS into the lungs, cell counts in the bronchoalveolar lavage fluid (BALF) were determined. Lung tissues were separated to assess the degree of inflammation, pulmonary oedema, epithelial apoptosis and the expression of ER stress marker proteins.Results: The 78-kDa glucose-regulated protein (GRP78) and C/EBP homologous protein (CHOP) expression in the lung tissues of obese rats was upregulated before ALI, as well as the elevated apoptosis in epithelial cells. During ALI, the expression of ER stress marker proteins was similarly increased in both lean and obese rats, while significant downregulation of Mitofusin 2 (MFN2) was detected in obese epithelial cells. The lung tissues of obese rats showed higher concentrations of tumor necrosis factor-alpha (TNF-α), Interleukin 6 (IL-6) and IL-10, enhanced neutrophil counts and elevated wet/dry weight ratios. APN and 4-PBA decreased the degree of ER stress and suppressed LPS-induced lung inflammation, pulmonary oedema and epithelial apoptosis.Conclusion: APN may exert protective effects against the exacerbated lung injuries in obese rats by attenuating ER stress, which operates as a key molecular pathway in the progression of ALI.Keywords: adiponectin, endoplasmic reticulum stress, obesity, lung injuryWei KLuo JCao JPeng LRen LZhang FDove Medical Pressarticleadiponectinendoplasmic reticulum stressobesitylung injurySpecialties of internal medicineRC581-951ENDiabetes, Metabolic Syndrome and Obesity: Targets and Therapy, Vol Volume 13, Pp 4179-4190 (2020)
institution	DOAJ
collection	DOAJ
language	EN
topic	adiponectin endoplasmic reticulum stress obesity lung injury Specialties of internal medicine RC581-951
spellingShingle	adiponectin endoplasmic reticulum stress obesity lung injury Specialties of internal medicine RC581-951 Wei K Luo J Cao J Peng L Ren L Zhang F Adiponectin Protects Obese Rats from Aggravated Acute Lung Injury via Suppression of Endoplasmic Reticulum Stress
description	Ke Wei,1 Jie Luo,1 Jun Cao,1 Lihua Peng,1 Li Ren,1 Fan Zhang2 1Department of Anesthesiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, People’s Republic of China; 2Department of Anesthesiology, Jianyang People’s Hospital, Jianyang, Sichuan 641400, People’s Republic of ChinaCorrespondence: Ke WeiDepartment of Anesthesiology, The First Affiliated Hospital of Chongqing Medical University, 1# Youyi Road, Yuzhong District, Chongqing, People’s Republic of ChinaTel +86 23 89011069Fax +86 23 89011062Email wk202448@hospital-cqmu.comIntroduction: Endoplasmic reticulum (ER) stress seems to mediate the obesity-induced susceptibility to acute lung injury (ALI). The present study was designed to evaluate the role of ER stress in adiponectin (APN)-induced lung protection in an obese rat model treated with lipopolysaccharide (LPS).Methods: Four-week-old male Sprague-Dawley rats fed either a normal chow diet or a high-fat diet for 12 weeks were randomly assigned to one of the following groups: lean rats, diet-induced obesity rats, lean rats with ALI, obese rats with ALI, obese rats pretreated with 4-phenylbutyric acid (4-PBA) before ALI or obese rats pretreated with APN before ALI. At 24 h after instillation of LPS into the lungs, cell counts in the bronchoalveolar lavage fluid (BALF) were determined. Lung tissues were separated to assess the degree of inflammation, pulmonary oedema, epithelial apoptosis and the expression of ER stress marker proteins.Results: The 78-kDa glucose-regulated protein (GRP78) and C/EBP homologous protein (CHOP) expression in the lung tissues of obese rats was upregulated before ALI, as well as the elevated apoptosis in epithelial cells. During ALI, the expression of ER stress marker proteins was similarly increased in both lean and obese rats, while significant downregulation of Mitofusin 2 (MFN2) was detected in obese epithelial cells. The lung tissues of obese rats showed higher concentrations of tumor necrosis factor-alpha (TNF-α), Interleukin 6 (IL-6) and IL-10, enhanced neutrophil counts and elevated wet/dry weight ratios. APN and 4-PBA decreased the degree of ER stress and suppressed LPS-induced lung inflammation, pulmonary oedema and epithelial apoptosis.Conclusion: APN may exert protective effects against the exacerbated lung injuries in obese rats by attenuating ER stress, which operates as a key molecular pathway in the progression of ALI.Keywords: adiponectin, endoplasmic reticulum stress, obesity, lung injury
format	article
author	Wei K Luo J Cao J Peng L Ren L Zhang F
author_facet	Wei K Luo J Cao J Peng L Ren L Zhang F
author_sort	Wei K
title	Adiponectin Protects Obese Rats from Aggravated Acute Lung Injury via Suppression of Endoplasmic Reticulum Stress
title_short	Adiponectin Protects Obese Rats from Aggravated Acute Lung Injury via Suppression of Endoplasmic Reticulum Stress
title_full	Adiponectin Protects Obese Rats from Aggravated Acute Lung Injury via Suppression of Endoplasmic Reticulum Stress
title_fullStr	Adiponectin Protects Obese Rats from Aggravated Acute Lung Injury via Suppression of Endoplasmic Reticulum Stress
title_full_unstemmed	Adiponectin Protects Obese Rats from Aggravated Acute Lung Injury via Suppression of Endoplasmic Reticulum Stress
title_sort	adiponectin protects obese rats from aggravated acute lung injury via suppression of endoplasmic reticulum stress
publisher	Dove Medical Press
publishDate	2020
url	https://doaj.org/article/4fa3433b35f24508a88178286455f991
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Adiponectin Protects Obese Rats from Aggravated Acute Lung Injury via Suppression of Endoplasmic Reticulum Stress

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