N-Acetyl Cysteine Inhibits Endothelin-1-Induced ROS Dependent Cardiac Hypertrophy through Superoxide Dismutase Regulation
Objective: Oxidative stress down regulates antioxidant enzymes including superoxide dismutase (SOD) and contributes to the development of cardiac hypertrophy. N-Acetyl cysteine (NAC) can enhance the SOD activity, so the aim of this study is to highlight the inhibitory role of NAC against endothel...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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Royan Institute (ACECR), Tehran
2015-07-01
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| Series: | Cell Journal |
| Subjects: | |
| Online Access: | http://celljournal.org/web/journal/article/391/download |
| _version_ | 1818251872369115136 |
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| author | Sobia Mushtaq Tahir Ali Qamar Javed Sobia Tabassum Iram Murtaza |
| author_facet | Sobia Mushtaq Tahir Ali Qamar Javed Sobia Tabassum Iram Murtaza |
| author_sort | Sobia Mushtaq |
| collection | DOAJ |
| description | Objective: Oxidative stress down regulates antioxidant enzymes including superoxide
dismutase (SOD) and contributes to the development of cardiac hypertrophy. N-Acetyl
cysteine (NAC) can enhance the SOD activity, so the aim of this study is to highlight the
inhibitory role of NAC against endothelin-1 (ET-1)-induced cardiac hypertrophy.
Materials and Methods: In this experimental study at QAU from January, 2013 to March,
2013. ET-1 (50 μg/kg) and NAC (50 mg/kg) were given intraperitoneally to 6-day old neonatal
rats in combination or alone. All rats were sacrificed 15 days after the final injection. Histological
analysis was carried out to observe the effects caused by both drugs. Reactive oxygen
species (ROS) analysis and SOD assay were also carried out. Expression level of hypertrophic
marker, brain natriuretic peptide (BNP), was detected by western blotting.
Results: Our findings showed that ET-1-induced cardiac hypertrophy leading towards
heart failure was due to the imbalance of different parameters including free radical-induced
oxidative stress and antioxidative enzymes such as SOD. Furthermore NAC acted
as an antioxidant and played inhibitory role against ROS-dependent hypertrophy via regulatory
role of SOD as a result of oxidative response associated with hypertrophy.
Conclusion: ET-1-induced hypertrophic response is associated with increased ROS production
and decreased SOD level, while NAC plays a role against free radicals-induced
oxidative stress via SOD regulation. |
| first_indexed | 2024-12-12T16:15:11Z |
| format | Article |
| id | doaj.art-00208e5fdc494920a9401f61d621fd01 |
| institution | Directory Open Access Journal |
| issn | 2228-5806 2228-5814 |
| language | English |
| last_indexed | 2024-12-12T16:15:11Z |
| publishDate | 2015-07-01 |
| publisher | Royan Institute (ACECR), Tehran |
| record_format | Article |
| series | Cell Journal |
| spelling | doaj.art-00208e5fdc494920a9401f61d621fd012022-12-22T00:19:05ZengRoyan Institute (ACECR), TehranCell Journal2228-58062228-58142015-07-01172355360N-Acetyl Cysteine Inhibits Endothelin-1-Induced ROS Dependent Cardiac Hypertrophy through Superoxide Dismutase RegulationSobia Mushtaq0Tahir Ali1Qamar Javed2Sobia Tabassum3Iram Murtaza4Department of Biochemistry, Quaid-i-Azam University, Islamabad, PakistanDepartment of Biochemistry, Quaid-i-Azam University, Islamabad, PakistanDepartment of Biochemistry, Quaid-i-Azam University, Islamabad, PakistanDepartment of Biotechnology, International Islamic University, Islamabad, PakistanDepartment of Biochemistry, Quaid-i-Azam University, Islamabad, PakistanObjective: Oxidative stress down regulates antioxidant enzymes including superoxide dismutase (SOD) and contributes to the development of cardiac hypertrophy. N-Acetyl cysteine (NAC) can enhance the SOD activity, so the aim of this study is to highlight the inhibitory role of NAC against endothelin-1 (ET-1)-induced cardiac hypertrophy. Materials and Methods: In this experimental study at QAU from January, 2013 to March, 2013. ET-1 (50 μg/kg) and NAC (50 mg/kg) were given intraperitoneally to 6-day old neonatal rats in combination or alone. All rats were sacrificed 15 days after the final injection. Histological analysis was carried out to observe the effects caused by both drugs. Reactive oxygen species (ROS) analysis and SOD assay were also carried out. Expression level of hypertrophic marker, brain natriuretic peptide (BNP), was detected by western blotting. Results: Our findings showed that ET-1-induced cardiac hypertrophy leading towards heart failure was due to the imbalance of different parameters including free radical-induced oxidative stress and antioxidative enzymes such as SOD. Furthermore NAC acted as an antioxidant and played inhibitory role against ROS-dependent hypertrophy via regulatory role of SOD as a result of oxidative response associated with hypertrophy. Conclusion: ET-1-induced hypertrophic response is associated with increased ROS production and decreased SOD level, while NAC plays a role against free radicals-induced oxidative stress via SOD regulation.http://celljournal.org/web/journal/article/391/downloadCardiac HypertrophyEndothelin-1Oxidative StressSuperoxide DismutaseReactive Oxygen Species |
| spellingShingle | Sobia Mushtaq Tahir Ali Qamar Javed Sobia Tabassum Iram Murtaza N-Acetyl Cysteine Inhibits Endothelin-1-Induced ROS Dependent Cardiac Hypertrophy through Superoxide Dismutase Regulation Cell Journal Cardiac Hypertrophy Endothelin-1 Oxidative Stress Superoxide Dismutase Reactive Oxygen Species |
| title | N-Acetyl Cysteine Inhibits Endothelin-1-Induced ROS Dependent Cardiac Hypertrophy through Superoxide Dismutase Regulation |
| title_full | N-Acetyl Cysteine Inhibits Endothelin-1-Induced ROS Dependent Cardiac Hypertrophy through Superoxide Dismutase Regulation |
| title_fullStr | N-Acetyl Cysteine Inhibits Endothelin-1-Induced ROS Dependent Cardiac Hypertrophy through Superoxide Dismutase Regulation |
| title_full_unstemmed | N-Acetyl Cysteine Inhibits Endothelin-1-Induced ROS Dependent Cardiac Hypertrophy through Superoxide Dismutase Regulation |
| title_short | N-Acetyl Cysteine Inhibits Endothelin-1-Induced ROS Dependent Cardiac Hypertrophy through Superoxide Dismutase Regulation |
| title_sort | n acetyl cysteine inhibits endothelin 1 induced ros dependent cardiac hypertrophy through superoxide dismutase regulation |
| topic | Cardiac Hypertrophy Endothelin-1 Oxidative Stress Superoxide Dismutase Reactive Oxygen Species |
| url | http://celljournal.org/web/journal/article/391/download |
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