Nerol protects against hypoxia/reoxygenation-induced apoptotic injury by activating PI3K/AKT signaling in cardiomyocytes

Background: Nerol was reported as a natural anti-oxidant product and its protective effects against cardiovascular diseases have been documented. Our current study was designed to explore the cardioprotective effect of Nerol on hypoxia/reoxygenation (H/R)-induced production of reactive oxygen specie...

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Main Authors: Jin Cheng, Qing Zou, Yugang Xue
Format: Article
Language:English
Published: Innovation Publishing House Pte. Ltd. 2021-03-01
Series:STEMedicine
Subjects:
Online Access:https://stemedicine.org/index.php/stem/article/view/87
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author Jin Cheng
Qing Zou
Yugang Xue
author_facet Jin Cheng
Qing Zou
Yugang Xue
author_sort Jin Cheng
collection DOAJ
description Background: Nerol was reported as a natural anti-oxidant product and its protective effects against cardiovascular diseases have been documented. Our current study was designed to explore the cardioprotective effect of Nerol on hypoxia/reoxygenation (H/R)-induced production of reactive oxygen species (ROS) and cell apoptosis in H9c2 cells. The potential molecular mechanisms were further investigated. Methods: The cells were treated with 2.5 or 5 µM Nerol before or after H/R. Lactate dehydrogenase (LDH) release, cell viability, oxidative stress markers, and apoptotic proteins were assessed by cell counting kit-8, LDH release assay, commercial kits, and Western blot, respectively. To explore the underlying mechanism, the phosphorylation of p85 and p38, regulatory subunits of phosphoinositide-3-kinase (PI3K)/protein kinase B (AKT) and mitogen-activated protein kinase (MAPK), was evaluated by Western blot. To further confirm that the PI3K/AKT signaling pathway participated in the cardiomyocyte protection, H9c2 cells were treated with 5 µM Nerol in the presence or absence of 5 µM BEZ235 or LY294002 followed by H/R treatment. Results: H/R remarkably induced apoptosis, LDH release and ROS production. The cell viability was suppressed via inhibiting the PI3K/AKT signaling pathway activation. By contrast, pretreatment with Nerol can neutralize these effects by activating the PI3K/AKT signaling pathway. With the addition of BEZ235 or LY294002, the inhibitory effects of Nerol were abolished. Conclusion: Nerol provided promising cardioprotective effect against H/R-induced injuries in H9c2 cells by activating the PI3K/AKT pathway.
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spelling doaj.art-8a863ed0bbe44a66943638928afe89b32022-12-21T23:08:54ZengInnovation Publishing House Pte. Ltd.STEMedicine2705-11882021-03-012610.37175/stemedicine.v2i6.87Nerol protects against hypoxia/reoxygenation-induced apoptotic injury by activating PI3K/AKT signaling in cardiomyocytesJin Cheng0Qing Zou1Yugang Xue2Department of Cardiology, Tangdu Hospital, Air force Military Medical University, Xi’an 710000, ChinaDepartment of Cardiology, Tangdu Hospital, Air force Military Medical University, Xi’an 710000, ChinaDepartment of Cardiology, Tangdu Hospital, Air force Military Medical University, Xi’an 710000, ChinaBackground: Nerol was reported as a natural anti-oxidant product and its protective effects against cardiovascular diseases have been documented. Our current study was designed to explore the cardioprotective effect of Nerol on hypoxia/reoxygenation (H/R)-induced production of reactive oxygen species (ROS) and cell apoptosis in H9c2 cells. The potential molecular mechanisms were further investigated. Methods: The cells were treated with 2.5 or 5 µM Nerol before or after H/R. Lactate dehydrogenase (LDH) release, cell viability, oxidative stress markers, and apoptotic proteins were assessed by cell counting kit-8, LDH release assay, commercial kits, and Western blot, respectively. To explore the underlying mechanism, the phosphorylation of p85 and p38, regulatory subunits of phosphoinositide-3-kinase (PI3K)/protein kinase B (AKT) and mitogen-activated protein kinase (MAPK), was evaluated by Western blot. To further confirm that the PI3K/AKT signaling pathway participated in the cardiomyocyte protection, H9c2 cells were treated with 5 µM Nerol in the presence or absence of 5 µM BEZ235 or LY294002 followed by H/R treatment. Results: H/R remarkably induced apoptosis, LDH release and ROS production. The cell viability was suppressed via inhibiting the PI3K/AKT signaling pathway activation. By contrast, pretreatment with Nerol can neutralize these effects by activating the PI3K/AKT signaling pathway. With the addition of BEZ235 or LY294002, the inhibitory effects of Nerol were abolished. Conclusion: Nerol provided promising cardioprotective effect against H/R-induced injuries in H9c2 cells by activating the PI3K/AKT pathway.https://stemedicine.org/index.php/stem/article/view/87NerolOxidative stressHypoxia/reoxygenationApoptosisPI3K/AKT signaling
spellingShingle Jin Cheng
Qing Zou
Yugang Xue
Nerol protects against hypoxia/reoxygenation-induced apoptotic injury by activating PI3K/AKT signaling in cardiomyocytes
STEMedicine
Nerol
Oxidative stress
Hypoxia/reoxygenation
Apoptosis
PI3K/AKT signaling
title Nerol protects against hypoxia/reoxygenation-induced apoptotic injury by activating PI3K/AKT signaling in cardiomyocytes
title_full Nerol protects against hypoxia/reoxygenation-induced apoptotic injury by activating PI3K/AKT signaling in cardiomyocytes
title_fullStr Nerol protects against hypoxia/reoxygenation-induced apoptotic injury by activating PI3K/AKT signaling in cardiomyocytes
title_full_unstemmed Nerol protects against hypoxia/reoxygenation-induced apoptotic injury by activating PI3K/AKT signaling in cardiomyocytes
title_short Nerol protects against hypoxia/reoxygenation-induced apoptotic injury by activating PI3K/AKT signaling in cardiomyocytes
title_sort nerol protects against hypoxia reoxygenation induced apoptotic injury by activating pi3k akt signaling in cardiomyocytes
topic Nerol
Oxidative stress
Hypoxia/reoxygenation
Apoptosis
PI3K/AKT signaling
url https://stemedicine.org/index.php/stem/article/view/87
work_keys_str_mv AT jincheng nerolprotectsagainsthypoxiareoxygenationinducedapoptoticinjurybyactivatingpi3kaktsignalingincardiomyocytes
AT qingzou nerolprotectsagainsthypoxiareoxygenationinducedapoptoticinjurybyactivatingpi3kaktsignalingincardiomyocytes
AT yugangxue nerolprotectsagainsthypoxiareoxygenationinducedapoptoticinjurybyactivatingpi3kaktsignalingincardiomyocytes