Propofol postconditioning ameliorates hypoxia/reoxygenation induced H9c2 cell apoptosis and autophagy via upregulating forkhead transcription factors under hyperglycemia

Abstract Background Administration of propofol, an intravenous anesthetic with antioxidant property, immediately at the onset of post-ischemic reperfusion (propofol postconditioning, P-PostC) has been shown to confer cardioprotection against ischemia–reperfusion injury, while the underlying mechanis...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Rong-Hui Han, He-Meng Huang, Hong Han, Hao Chen, Fei Zeng, Xiang Xie, Dan-Yong Liu, Yin Cai, Liang-Qing Zhang, Xin Liu, Zheng-Yuan Xia, Jing Tang
Formato:	article
Lenguaje:	EN
Publicado:	BMC 2021
Materias:	H/R injury Hyperglycemia P-PostC Apoptosis Autophagy FoxO Medicine (General) R5-920 Military Science U
Acceso en línea:	https://doaj.org/article/2aaabbf8f80f47518055e4944a2e55db
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:2aaabbf8f80f47518055e4944a2e55db
record_format	dspace
spelling	oai:doaj.org-article:2aaabbf8f80f47518055e4944a2e55db2021-11-14T12:28:58ZPropofol postconditioning ameliorates hypoxia/reoxygenation induced H9c2 cell apoptosis and autophagy via upregulating forkhead transcription factors under hyperglycemia10.1186/s40779-021-00353-02054-9369https://doaj.org/article/2aaabbf8f80f47518055e4944a2e55db2021-11-01T00:00:00Zhttps://doi.org/10.1186/s40779-021-00353-0https://doaj.org/toc/2054-9369Abstract Background Administration of propofol, an intravenous anesthetic with antioxidant property, immediately at the onset of post-ischemic reperfusion (propofol postconditioning, P-PostC) has been shown to confer cardioprotection against ischemia–reperfusion injury, while the underlying mechanism remains incompletely understood. The FoxO transcription factors are reported to play critical roles in activating cardiomyocyte survival signaling throughout the process of cellular injuries induced by oxidative stress and are also involved in hypoxic postconditioning mediated neuroprotection, however, the role of FoxO in postconditioning mediated protection in the heart and in particular in high glucose condition is unknown. Methods Rat heart-derived H9c2 cells were exposed to high glucose (HG) for 48 h (h), then subjected to hypoxia/reoxygenation (H/R, composed of 8 h of hypoxia followed by 12 h of reoxygenation) in the absence or presence of postconditioning with various concentrations of propofol (P-PostC) at the onset of reoxygenation. After having identified the optical concentration of propofol, H9c2 cells were subjected to H/R and P-PostC in the absence or presence of FoxO1 or FoxO3a gene silencing to explore their roles in P-PostC mediated protection against apoptotic and autophagic cell deaths under hyperglycemia. Results The results showed that HG with or without H/R decreased cell viability, increased lactate dehydrogenase (LDH) leakage and the production of reactive oxygen species (ROS) in H9c2 cells, all of which were significantly reversed by propofol (P-PostC), especially at the concentration of 25 µmol/L (P25) (all P < 0.05, NC vs. HG; HG vs. HG + HR; HG + HR + P12.5 or HG + HR + P25 or HG + HR + P50 vs. HG + HR). Moreover, we found that propofol (P25) decreased H9c2 cells apoptosis and autophagy that were concomitant with increased FoxO1 and FoxO3a expression (all P < 0.05, HG + HR + P25 vs. HG + HR). The protective effects of propofol (P25) against H/R injury were reversed by silencing FoxO1 or FoxO3a (all P < 0.05, HG + HR + P25 vs. HG + HR + P25 + siRNA-1 or HG + HR + P25 + siRNA-5). Conclusion It is concluded that propofol postconditioning attenuated H9c2 cardiac cells apoptosis and autophagy induced by H/R injury through upregulating FoxO1 and FoxO3a under hyperglycemia.Rong-Hui HanHe-Meng HuangHong HanHao ChenFei ZengXiang XieDan-Yong LiuYin CaiLiang-Qing ZhangXin LiuZheng-Yuan XiaJing TangBMCarticleH/R injuryHyperglycemiaP-PostCApoptosisAutophagyFoxOMedicine (General)R5-920Military ScienceUENMilitary Medical Research, Vol 8, Iss 1, Pp 1-16 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	H/R injury Hyperglycemia P-PostC Apoptosis Autophagy FoxO Medicine (General) R5-920 Military Science U
spellingShingle	H/R injury Hyperglycemia P-PostC Apoptosis Autophagy FoxO Medicine (General) R5-920 Military Science U Rong-Hui Han He-Meng Huang Hong Han Hao Chen Fei Zeng Xiang Xie Dan-Yong Liu Yin Cai Liang-Qing Zhang Xin Liu Zheng-Yuan Xia Jing Tang Propofol postconditioning ameliorates hypoxia/reoxygenation induced H9c2 cell apoptosis and autophagy via upregulating forkhead transcription factors under hyperglycemia
description	Abstract Background Administration of propofol, an intravenous anesthetic with antioxidant property, immediately at the onset of post-ischemic reperfusion (propofol postconditioning, P-PostC) has been shown to confer cardioprotection against ischemia–reperfusion injury, while the underlying mechanism remains incompletely understood. The FoxO transcription factors are reported to play critical roles in activating cardiomyocyte survival signaling throughout the process of cellular injuries induced by oxidative stress and are also involved in hypoxic postconditioning mediated neuroprotection, however, the role of FoxO in postconditioning mediated protection in the heart and in particular in high glucose condition is unknown. Methods Rat heart-derived H9c2 cells were exposed to high glucose (HG) for 48 h (h), then subjected to hypoxia/reoxygenation (H/R, composed of 8 h of hypoxia followed by 12 h of reoxygenation) in the absence or presence of postconditioning with various concentrations of propofol (P-PostC) at the onset of reoxygenation. After having identified the optical concentration of propofol, H9c2 cells were subjected to H/R and P-PostC in the absence or presence of FoxO1 or FoxO3a gene silencing to explore their roles in P-PostC mediated protection against apoptotic and autophagic cell deaths under hyperglycemia. Results The results showed that HG with or without H/R decreased cell viability, increased lactate dehydrogenase (LDH) leakage and the production of reactive oxygen species (ROS) in H9c2 cells, all of which were significantly reversed by propofol (P-PostC), especially at the concentration of 25 µmol/L (P25) (all P < 0.05, NC vs. HG; HG vs. HG + HR; HG + HR + P12.5 or HG + HR + P25 or HG + HR + P50 vs. HG + HR). Moreover, we found that propofol (P25) decreased H9c2 cells apoptosis and autophagy that were concomitant with increased FoxO1 and FoxO3a expression (all P < 0.05, HG + HR + P25 vs. HG + HR). The protective effects of propofol (P25) against H/R injury were reversed by silencing FoxO1 or FoxO3a (all P < 0.05, HG + HR + P25 vs. HG + HR + P25 + siRNA-1 or HG + HR + P25 + siRNA-5). Conclusion It is concluded that propofol postconditioning attenuated H9c2 cardiac cells apoptosis and autophagy induced by H/R injury through upregulating FoxO1 and FoxO3a under hyperglycemia.
format	article
author	Rong-Hui Han He-Meng Huang Hong Han Hao Chen Fei Zeng Xiang Xie Dan-Yong Liu Yin Cai Liang-Qing Zhang Xin Liu Zheng-Yuan Xia Jing Tang
author_facet	Rong-Hui Han He-Meng Huang Hong Han Hao Chen Fei Zeng Xiang Xie Dan-Yong Liu Yin Cai Liang-Qing Zhang Xin Liu Zheng-Yuan Xia Jing Tang
author_sort	Rong-Hui Han
title	Propofol postconditioning ameliorates hypoxia/reoxygenation induced H9c2 cell apoptosis and autophagy via upregulating forkhead transcription factors under hyperglycemia
title_short	Propofol postconditioning ameliorates hypoxia/reoxygenation induced H9c2 cell apoptosis and autophagy via upregulating forkhead transcription factors under hyperglycemia
title_full	Propofol postconditioning ameliorates hypoxia/reoxygenation induced H9c2 cell apoptosis and autophagy via upregulating forkhead transcription factors under hyperglycemia
title_fullStr	Propofol postconditioning ameliorates hypoxia/reoxygenation induced H9c2 cell apoptosis and autophagy via upregulating forkhead transcription factors under hyperglycemia
title_full_unstemmed	Propofol postconditioning ameliorates hypoxia/reoxygenation induced H9c2 cell apoptosis and autophagy via upregulating forkhead transcription factors under hyperglycemia
title_sort	propofol postconditioning ameliorates hypoxia/reoxygenation induced h9c2 cell apoptosis and autophagy via upregulating forkhead transcription factors under hyperglycemia
publisher	BMC
publishDate	2021
url	https://doaj.org/article/2aaabbf8f80f47518055e4944a2e55db
work_keys_str_mv	AT ronghuihan propofolpostconditioningameliorateshypoxiareoxygenationinducedh9c2cellapoptosisandautophagyviaupregulatingforkheadtranscriptionfactorsunderhyperglycemia AT hemenghuang propofolpostconditioningameliorateshypoxiareoxygenationinducedh9c2cellapoptosisandautophagyviaupregulatingforkheadtranscriptionfactorsunderhyperglycemia AT honghan propofolpostconditioningameliorateshypoxiareoxygenationinducedh9c2cellapoptosisandautophagyviaupregulatingforkheadtranscriptionfactorsunderhyperglycemia AT haochen propofolpostconditioningameliorateshypoxiareoxygenationinducedh9c2cellapoptosisandautophagyviaupregulatingforkheadtranscriptionfactorsunderhyperglycemia AT feizeng propofolpostconditioningameliorateshypoxiareoxygenationinducedh9c2cellapoptosisandautophagyviaupregulatingforkheadtranscriptionfactorsunderhyperglycemia AT xiangxie propofolpostconditioningameliorateshypoxiareoxygenationinducedh9c2cellapoptosisandautophagyviaupregulatingforkheadtranscriptionfactorsunderhyperglycemia AT danyongliu propofolpostconditioningameliorateshypoxiareoxygenationinducedh9c2cellapoptosisandautophagyviaupregulatingforkheadtranscriptionfactorsunderhyperglycemia AT yincai propofolpostconditioningameliorateshypoxiareoxygenationinducedh9c2cellapoptosisandautophagyviaupregulatingforkheadtranscriptionfactorsunderhyperglycemia AT liangqingzhang propofolpostconditioningameliorateshypoxiareoxygenationinducedh9c2cellapoptosisandautophagyviaupregulatingforkheadtranscriptionfactorsunderhyperglycemia AT xinliu propofolpostconditioningameliorateshypoxiareoxygenationinducedh9c2cellapoptosisandautophagyviaupregulatingforkheadtranscriptionfactorsunderhyperglycemia AT zhengyuanxia propofolpostconditioningameliorateshypoxiareoxygenationinducedh9c2cellapoptosisandautophagyviaupregulatingforkheadtranscriptionfactorsunderhyperglycemia AT jingtang propofolpostconditioningameliorateshypoxiareoxygenationinducedh9c2cellapoptosisandautophagyviaupregulatingforkheadtranscriptionfactorsunderhyperglycemia
_version_	1718429156374478848

Propofol postconditioning ameliorates hypoxia/reoxygenation induced H9c2 cell apoptosis and autophagy via upregulating forkhead transcription factors under hyperglycemia

Ejemplares similares