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Background: Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Nox) is one of the predominant sources of the production of free oxygen radicals in the vascular wall. Endothelin-1 is a potent vasoconstrictor factor that also has mitogenic activity in vascular smooth muscle cells. The activation of transforming growth factor beta (TGF–β) receptor by endothelin-1 plays an important role in cardiovascular diseases. The aim of this study was to investigate the changes of Nox gene expression in smooth muscle cells treated with endothelin-1 in the presence of the transforming growth factor beta-receptor antagonist. Methods: Human aortic smooth muscle cells (HA-SMCs) were treated with endothelin-1 (100 nM) and transforming growth factor beta (2 ng/ml) in the presence and absence of transforming growth factor beta-receptor antagonist. The mRNA expression of Nox1 and Nox4 were assessed using real-time polymerase chain reaction (PCR) technique. Findings: The gene expression of Nox1 increased in the presence of endothelin-1 compared to control group, but there was no change in gene expression of Nox4. Increasing the expression of Nox1 decreased in the presence of transforming growth factor beta-receptor antagonist (10 μM). Conclusion: The results of this study showed that activation of transforming growth factor beta pathway is one of the mechanisms for increasing the mRNA expression of Nox1 by endothelin-1.

Background & Objective: NFκB is a dimeric transcription factor with multiple subunits. Phosphorylation of p65 (one of NFκB subunits) by oxidative stress leads to the activation of NFκB. Imbalance between oxidative stress and cellular antioxidant capacity is the pathogenesis of many diseases. Consuming antioxidants in daily meal can be considered as a preventive strategy for inflammatory diseases. Among antioxidant components, curcumin is a natural polyphenol which is extracted from Tumeric. Curcumin can protect the human body from oxidative stress by neutralizing the free radicals. Material & Methods: Bovine Endothelial Cells (BECs) were treated with different concentration of H2O2 (10, 20, 80, 200 μM). To investigate the inhibitory effect of curcumin on H2O2 mediated phosphorylation of p65, BECs were incubated with 5 and 10μM concentration of curcumin. Protein concentration was measured by Bradford method and phosphorylation of p65 was assessed by western blotting. Results: Our finding indicated that p65 phosphorylation was increased two fold in presence of H2O2 (200 μM) in comparison with control. The enhancing effect of H2O2 on p65 phosphorylation decreased at 30 min (P: 0.03) and 2 hours (P:0.015) after treatment with 10 μM dose of curcumin. Conclusion: The result of this study indicates that one of anti-inflammatory mechanisms of curcumin is through NFκB pathway by inhibition of p65 subunit phosphorylation.