Sulforaphane improves redox homeostasis and right ventricular contractility in a model of pulmonary hypertension
Pulmonary arterial hypertension (PAH) is characterized by increased pulmonary vascular resistance, imposing overload on the right ventricle (RV) and imbalance of redox state. Our study investigated the influence of treatment with sulforaphane (SFN), found in cruciferous vegetables, on right ventricl...
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| Published in: | Journal of cardiovascular pharmacology Vol. 83; no. 6; pp. 612 - 620 |
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| Abstract | Pulmonary arterial hypertension (PAH) is characterized by increased pulmonary vascular resistance, imposing overload on the right ventricle (RV) and imbalance of redox state. Our study investigated the influence of treatment with sulforaphane (SFN), found in cruciferous vegetables, on right ventricle (RV) remodeling and redox homeostasis in monocrotaline-induced pulmonary arterial hypertension (PAH). Male Wistar rats were separated into four groups: control (CTR); control + sulforaphane (CTR + SFN); monocrotaline (MCT); monocrotaline + sulforaphane (MCT + SFN). PAH induction was implemented by a single dose of MCT (60 mg/kg i.p.). Treatment with SFN (2.5 mg/kg/day i.p.) started on the 7th day after the MCT injection and persisted for 2 weeks. After 21 days of PAH induction, echocardiography, hemodynamic, and oxidative stress evaluation were performed. MCT group showed increase in RV hypertrophy, RV systolic area, RV systolic, mean pulmonary artery pressure (mPAP), and pulmonary vascular resistance (PVR), while exhibited a decrease in RV outflow tract AT/ET ratio, RV fractional shortening and tricuspid annular plane systolic excursion (TAPSE) compared to CTR (P<0.05). SFN-treated PAH attenuated detrimental changes in TPSE, mPAP, and PVR parameters. Catalase and GSH/GSSG ratio were diminished in MCT compared to CTR (P<0.05). SFN increased catalase and normalized GSH/GSSG ratio to control levels (P<0.05). Data express a benefit of SFN treatment on the cardiac function of rats with PAH associated with the cellular redox state. |
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| AbstractList | Pulmonary arterial hypertension (PAH) is characterized by increased pulmonary vascular resistance (PVR), imposing overload on the right ventricle (RV) and imbalance of the redox state. Our study investigated the influence of treatment with sulforaphane (SFN), found in cruciferous vegetables, on RV remodeling and redox homeostasis in monocrotaline (MCT)-induced PAH. Male Wistar rats were separated into 4 groups: control (CTR); CTR + SFN; MCT; and MCT + SFN. PAH induction was implemented by a single dose of MCT (60 mg/kg intraperitoneally). Treatment with SFN (2.5 mg/kg/day intraperitoneally) started on the seventh day after the MCT injection and persisted for 2 weeks. After 21 days of PAH induction, echocardiographic, hemodynamic, and oxidative stress evaluation was performed. The MCT group showed an increase in RV hypertrophy, RV systolic area, RV systolic, mean pulmonary artery pressure, and PVR and exhibited a decrease in the RV outflow tract acceleration time/ejection time ratio, RV fractional shortening, and tricuspid annular plane systolic excursion compared to CTR ( P < 0.05). SFN-treated PAH attenuated detrimental changes in tricuspid annular plane systolic excursion, mean pulmonary artery pressure, and PVR parameters. Catalase levels and the glutathione/Glutathione disulfide (GSSG) ratio were diminished in the MCT group compared to CTR ( P < 0.05). SFN increased catalase levels and normalized the glutathione/GSSG ratio to control levels ( P < 0.05). Data express the benefit of SFN treatment on the cardiac function of rats with PAH associated with the cellular redox state.ABSTRACTPulmonary arterial hypertension (PAH) is characterized by increased pulmonary vascular resistance (PVR), imposing overload on the right ventricle (RV) and imbalance of the redox state. Our study investigated the influence of treatment with sulforaphane (SFN), found in cruciferous vegetables, on RV remodeling and redox homeostasis in monocrotaline (MCT)-induced PAH. Male Wistar rats were separated into 4 groups: control (CTR); CTR + SFN; MCT; and MCT + SFN. PAH induction was implemented by a single dose of MCT (60 mg/kg intraperitoneally). Treatment with SFN (2.5 mg/kg/day intraperitoneally) started on the seventh day after the MCT injection and persisted for 2 weeks. After 21 days of PAH induction, echocardiographic, hemodynamic, and oxidative stress evaluation was performed. The MCT group showed an increase in RV hypertrophy, RV systolic area, RV systolic, mean pulmonary artery pressure, and PVR and exhibited a decrease in the RV outflow tract acceleration time/ejection time ratio, RV fractional shortening, and tricuspid annular plane systolic excursion compared to CTR ( P < 0.05). SFN-treated PAH attenuated detrimental changes in tricuspid annular plane systolic excursion, mean pulmonary artery pressure, and PVR parameters. Catalase levels and the glutathione/Glutathione disulfide (GSSG) ratio were diminished in the MCT group compared to CTR ( P < 0.05). SFN increased catalase levels and normalized the glutathione/GSSG ratio to control levels ( P < 0.05). Data express the benefit of SFN treatment on the cardiac function of rats with PAH associated with the cellular redox state. Pulmonary arterial hypertension (PAH) is characterized by increased pulmonary vascular resistance (PVR), imposing overload on the right ventricle (RV) and imbalance of the redox state. Our study investigated the influence of treatment with sulforaphane (SFN), found in cruciferous vegetables, on RV remodeling and redox homeostasis in monocrotaline (MCT)-induced PAH. Male Wistar rats were separated into 4 groups: control (CTR); CTR + SFN; MCT; and MCT + SFN. PAH induction was implemented by a single dose of MCT (60 mg/kg intraperitoneally). Treatment with SFN (2.5 mg/kg/day intraperitoneally) started on the seventh day after the MCT injection and persisted for 2 weeks. After 21 days of PAH induction, echocardiographic, hemodynamic, and oxidative stress evaluation was performed. The MCT group showed an increase in RV hypertrophy, RV systolic area, RV systolic, mean pulmonary artery pressure, and PVR and exhibited a decrease in the RV outflow tract acceleration time/ejection time ratio, RV fractional shortening, and tricuspid annular plane systolic excursion compared to CTR ( P < 0.05). SFN-treated PAH attenuated detrimental changes in tricuspid annular plane systolic excursion, mean pulmonary artery pressure, and PVR parameters. Catalase levels and the glutathione/Glutathione disulfide (GSSG) ratio were diminished in the MCT group compared to CTR ( P < 0.05). SFN increased catalase levels and normalized the glutathione/GSSG ratio to control levels ( P < 0.05). Data express the benefit of SFN treatment on the cardiac function of rats with PAH associated with the cellular redox state. Pulmonary arterial hypertension (PAH) is characterized by increased pulmonary vascular resistance, imposing overload on the right ventricle (RV) and imbalance of redox state. Our study investigated the influence of treatment with sulforaphane (SFN), found in cruciferous vegetables, on right ventricle (RV) remodeling and redox homeostasis in monocrotaline-induced pulmonary arterial hypertension (PAH). Male Wistar rats were separated into four groups: control (CTR); control + sulforaphane (CTR + SFN); monocrotaline (MCT); monocrotaline + sulforaphane (MCT + SFN). PAH induction was implemented by a single dose of MCT (60 mg/kg i.p.). Treatment with SFN (2.5 mg/kg/day i.p.) started on the 7th day after the MCT injection and persisted for 2 weeks. After 21 days of PAH induction, echocardiography, hemodynamic, and oxidative stress evaluation were performed. MCT group showed increase in RV hypertrophy, RV systolic area, RV systolic, mean pulmonary artery pressure (mPAP), and pulmonary vascular resistance (PVR), while exhibited a decrease in RV outflow tract AT/ET ratio, RV fractional shortening and tricuspid annular plane systolic excursion (TAPSE) compared to CTR (P<0.05). SFN-treated PAH attenuated detrimental changes in TPSE, mPAP, and PVR parameters. Catalase and GSH/GSSG ratio were diminished in MCT compared to CTR (P<0.05). SFN increased catalase and normalized GSH/GSSG ratio to control levels (P<0.05). Data express a benefit of SFN treatment on the cardiac function of rats with PAH associated with the cellular redox state. |
| Author | Turck, Patrick Belló-Klein, Adriane Conzatti, Adriana Sander da Rosa Araujo, Alex Colombo, Rafael Luz de Castro, Alexandre Siqueira, Rafaela Campos-Carraro, Cristina |
| Author_xml | – sequence: 1 givenname: Adriana surname: Conzatti fullname: Conzatti, Adriana organization: Laboratory of Cardiovascular Physiology, Universidade Federal do Rio Grande do Sul - UFRGS, Porto Alegre, RS, Brasil – sequence: 2 givenname: Rafael surname: Colombo fullname: Colombo, Rafael – sequence: 3 givenname: Rafaela surname: Siqueira fullname: Siqueira, Rafaela – sequence: 4 givenname: Cristina surname: Campos-Carraro fullname: Campos-Carraro, Cristina – sequence: 5 givenname: Patrick surname: Turck fullname: Turck, Patrick – sequence: 6 givenname: Alexandre surname: Luz de Castro fullname: Luz de Castro, Alexandre – sequence: 7 givenname: Adriane surname: Belló-Klein fullname: Belló-Klein, Adriane – sequence: 8 givenname: Alex orcidid: 0000-0002-9482-7388 surname: Sander da Rosa Araujo fullname: Sander da Rosa Araujo, Alex |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/38547510$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1007/978-3-319-63245-2_14 10.1016/j.pupt.2015.09.007 10.1007/s11010-019-03652-2 10.1016/j.jnutbio.2016.05.004 10.1016/S0076-6879(84)05016-3 10.3109/01902148.2011.591892 10.1016/j.joim.2023.08.002 10.1111/bph.13948 10.1038/s41569-019-0260-8 10.1161/CIRCRESAHA.113.301129 10.1016/j.freeradbiomed.2020.12.452 10.1007/s00394-021-02642-9 10.1016/0022-1759(80)90340-3 10.1097/FJC.0b013e3181c87a9d 10.1089/ars.2012.4568 10.1023/B:MCBI.0000026047.48534.50 10.2174/0929867324666170428103206 10.1007/s10557-022-07323-1 10.1016/j.ab.2019.03.010 10.3390/molecules27123724 10.1016/j.vph.2016.06.006 10.1007/s00018-016-2223-0 10.1183/13993003.02334-2021 10.1007/s10067-022-06446-y 10.1016/S0076-6879(81)77050-2 10.1007/s10522-022-09984-9 10.1016/0076-6879(90)86093-B 10.1371/journal.ppat.1011506 10.1016/j.rmr.2019.10.012 10.1007/s11010-014-2292-z 10.1139/cjpp-2015-0282 10.3390/cells8020194 |
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