Effect of sulphoraphane on newborn mouse cardiomyocytes undergoing ischaemia/reperfusion injury

Context: Sulphoraphane (SFN) is an isothiocyanate, having antioxidant activity, antitumor, and therapeutic effects on cardiovascular disease. Objective: This study explores the mechanisms of SFN preconditioning on ischaemia/reperfusion injury (IRI). Materials and methods: Cardiomyocytes were divided...

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Autores principales: Na Peng, Luping Jin, Aizhen He, Changjin Deng, Xiaoqin Wang
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Publicado: Taylor & Francis Group 2019
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spelling oai:doaj.org-article:93e618c0660744bd83ff35f0d950689d2021-11-17T14:21:56ZEffect of sulphoraphane on newborn mouse cardiomyocytes undergoing ischaemia/reperfusion injury1388-02091744-511610.1080/13880209.2019.1680705https://doaj.org/article/93e618c0660744bd83ff35f0d950689d2019-01-01T00:00:00Zhttp://dx.doi.org/10.1080/13880209.2019.1680705https://doaj.org/toc/1388-0209https://doaj.org/toc/1744-5116Context: Sulphoraphane (SFN) is an isothiocyanate, having antioxidant activity, antitumor, and therapeutic effects on cardiovascular disease. Objective: This study explores the mechanisms of SFN preconditioning on ischaemia/reperfusion injury (IRI). Materials and methods: Cardiomyocytes were divided into four groups as follows: control group (normoxic condition), SFN group (5 μmol/L), hypoxia/reoxygenation (H/R) group (1 h, 3 h) and SFN + H/R group. Cell viability was determined by MTT method. Levels of creatine kinase (CK), nitric oxide (NO), superoxide dismutase (SOD) and maleic dialdehyde (MDA) were determined by colorimetric method. Cell apoptosis, levels of reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were determined by flow cytometry. Levels of Bax, Bcl-2, C caspase-3, NF-E2-related factor 2 (Nrf2) and haem oxygenase-1 (HO-1) were detected by Western blot. Results: H/R model inhibited cell viability, increased the levels of LDH, CK, Bax and C caspase-3, and decreased the levels of NO, Bcl-2, while the effect of H/R was partially reversed by SFN. SFN treatment reduced ROS, MDA (from 4.9 nM to 2.8 nM) production, elevated SOD level (from 39.5 U/mL to 61.7 U/mL) and improved MMP damage. Under the effect of SFN, up-regulation of nuclear Nrf2 expression and down-regulation of cytosolic Nrf2 expression were observed, which led to Nrf2 nuclear translocation and enhanced the expression of HO-1. Conclusion: These results suggested that SFN had a protective effect on cardiomyocytes undergoing IRI, and its mechanism may be realized via activating the Nrf2/HO-1 pathway, thereby inhibiting apoptosis. This might provide a new approach for the treatment of ischaemic heart disease.Na PengLuping JinAizhen HeChangjin DengXiaoqin WangTaylor & Francis Grouparticlenrf2/ho-1oxidative stressapoptosisreactive oxygen speciesmitochondrial membrane potentialTherapeutics. PharmacologyRM1-950ENPharmaceutical Biology, Vol 57, Iss 1, Pp 753-759 (2019)
institution DOAJ
collection DOAJ
language EN
topic nrf2/ho-1
oxidative stress
apoptosis
reactive oxygen species
mitochondrial membrane potential
Therapeutics. Pharmacology
RM1-950
spellingShingle nrf2/ho-1
oxidative stress
apoptosis
reactive oxygen species
mitochondrial membrane potential
Therapeutics. Pharmacology
RM1-950
Na Peng
Luping Jin
Aizhen He
Changjin Deng
Xiaoqin Wang
Effect of sulphoraphane on newborn mouse cardiomyocytes undergoing ischaemia/reperfusion injury
description Context: Sulphoraphane (SFN) is an isothiocyanate, having antioxidant activity, antitumor, and therapeutic effects on cardiovascular disease. Objective: This study explores the mechanisms of SFN preconditioning on ischaemia/reperfusion injury (IRI). Materials and methods: Cardiomyocytes were divided into four groups as follows: control group (normoxic condition), SFN group (5 μmol/L), hypoxia/reoxygenation (H/R) group (1 h, 3 h) and SFN + H/R group. Cell viability was determined by MTT method. Levels of creatine kinase (CK), nitric oxide (NO), superoxide dismutase (SOD) and maleic dialdehyde (MDA) were determined by colorimetric method. Cell apoptosis, levels of reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were determined by flow cytometry. Levels of Bax, Bcl-2, C caspase-3, NF-E2-related factor 2 (Nrf2) and haem oxygenase-1 (HO-1) were detected by Western blot. Results: H/R model inhibited cell viability, increased the levels of LDH, CK, Bax and C caspase-3, and decreased the levels of NO, Bcl-2, while the effect of H/R was partially reversed by SFN. SFN treatment reduced ROS, MDA (from 4.9 nM to 2.8 nM) production, elevated SOD level (from 39.5 U/mL to 61.7 U/mL) and improved MMP damage. Under the effect of SFN, up-regulation of nuclear Nrf2 expression and down-regulation of cytosolic Nrf2 expression were observed, which led to Nrf2 nuclear translocation and enhanced the expression of HO-1. Conclusion: These results suggested that SFN had a protective effect on cardiomyocytes undergoing IRI, and its mechanism may be realized via activating the Nrf2/HO-1 pathway, thereby inhibiting apoptosis. This might provide a new approach for the treatment of ischaemic heart disease.
format article
author Na Peng
Luping Jin
Aizhen He
Changjin Deng
Xiaoqin Wang
author_facet Na Peng
Luping Jin
Aizhen He
Changjin Deng
Xiaoqin Wang
author_sort Na Peng
title Effect of sulphoraphane on newborn mouse cardiomyocytes undergoing ischaemia/reperfusion injury
title_short Effect of sulphoraphane on newborn mouse cardiomyocytes undergoing ischaemia/reperfusion injury
title_full Effect of sulphoraphane on newborn mouse cardiomyocytes undergoing ischaemia/reperfusion injury
title_fullStr Effect of sulphoraphane on newborn mouse cardiomyocytes undergoing ischaemia/reperfusion injury
title_full_unstemmed Effect of sulphoraphane on newborn mouse cardiomyocytes undergoing ischaemia/reperfusion injury
title_sort effect of sulphoraphane on newborn mouse cardiomyocytes undergoing ischaemia/reperfusion injury
publisher Taylor & Francis Group
publishDate 2019
url https://doaj.org/article/93e618c0660744bd83ff35f0d950689d
work_keys_str_mv AT napeng effectofsulphoraphaneonnewbornmousecardiomyocytesundergoingischaemiareperfusioninjury
AT lupingjin effectofsulphoraphaneonnewbornmousecardiomyocytesundergoingischaemiareperfusioninjury
AT aizhenhe effectofsulphoraphaneonnewbornmousecardiomyocytesundergoingischaemiareperfusioninjury
AT changjindeng effectofsulphoraphaneonnewbornmousecardiomyocytesundergoingischaemiareperfusioninjury
AT xiaoqinwang effectofsulphoraphaneonnewbornmousecardiomyocytesundergoingischaemiareperfusioninjury
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