N-Acetyl Cysteine Inhibits Endothelin-1-Induced ROS Dependent Cardiac Hypertrophy through Superoxide Dismutase Regulation

(Pages: 355-360)
Sobia Mushtaq, M.Sc, 1Tahir Ali, M.Sc, 1Qamar Javed, Ph.D, 1Sobia Tabassum, Ph.D, 2Iram Murtaza, Ph.D, 1,*
Department of Biochemistry, Quaid-i-Azam University, Islamabad, 45320, Pakistan
Department of Biotechnology, International Islamic University, Islamabad, Pakistan
Department of Biochemistry, Quaid-i-Azam University, Islamabad, 45320, Pakistan
Department of Biotechnology, International Islamic University, Islamabad, Pakistan
*Corresponding Address: Department of Biochemistry Quaid-i-Azam University Islamabad 45320 Pakistan Email:iram_murtaza@hotmail.com
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Mushtaq Sobia, Ali Tahir, Javed Qamar, Tabassum Sobia, Murtaza Iram. N-Acetyl Cysteine Inhibits Endothelin-1-Induced ROS Dependent Cardiac Hypertrophy through Superoxide Dismutase Regulation. Cell J. 2015; 17(2): 355-360.

Abstract

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 hyper- trophic 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.