N-Acetyl Cysteine Inhibits Endothelin-1-Induced Ros Dependent Cardiac Hypertrophy Through Superoxide Dismutase Regulation

Objective: oxidative stress down regulates antioxidant enzymes including superoxidedismutase (sod) and contributes to the development of cardiac hypertrophy. n-acetylcysteine (nac) can enhance the sod activity, so the aim of this study is to highlight theinhibitory 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 ?g/kg) and nac (50 mg/kg) were given intraperitoneally to 6-day old neonatalrats in combination or alone. all rats were sacrificed 15 days after the final injection. histologicalanalysis was carried out to observe the effects caused by both drugs. reactive oxygenspecies (ros) analysis and sod assay were also carried out. expression level of hypertrophicmarker, brain natriuretic peptide (bnp), was detected by western blotting.results: our findings showed that et-1-induced cardiac hypertrophy leading towardsheart failure was due to the imbalance of different parameters including free radical-inducedoxidative stress and antioxidative enzymes such as sod. furthermore nac actedas an antioxidant and played inhibitory role against ros-dependent hypertrophy via regulatoryrole of sod as a result of oxidative response associated with hypertrophy.conclusion: et-1-induced hypertrophic response is associated with increased ros productionand decreased sod level, while nac plays a role against free radicals-inducedoxidative stress via sod regulation.