NAC is hypothesized to have numerous therapeutic benefits in the management of cardiovascular diseases, including post-AMI cardiac remodeling [16–18]. In animal models of GSK2126458 molecular weight ischemia and reperfusion,

NAC decreased infarct size [19, 20]. In combination with thrombolytics, NAC reduced oxidative stress, induced a trend toward more rapid reperfusion, and enhanced preservation of LV function [21, 22]. Although glutathione is considered to have a major role in preserving body homeostasis and protecting cells against toxic agents, it is not transported well into cells due to its large molecular size. Moreover, l-cysteine, the amino acid involved in the intracellular synthesis of glutathione, is toxic to humans. NAC can easily be deacetylated in cells to provide l-cysteine and therefore increase the intracellular glutathione concentration. Glutathione is a necessary factor for the activation of T lymphocytes and polymorphonuclear leukocytes in addition to cytokine production

[23]. As nuclear factor (NF)-κB has a role in INK 128 ic50 the inducible transcription of TNF-α and oxidative stress can induce its nuclear translocation, antioxidants including NAC can act as potent inhibitors of NF-κB activation [24, 25]. This may be the explanation behind how NAC might prevent the production of TNF-α. With respect to TGF-β, NAC can change this cytokine to its biologically inactive form and inhibit its binding to the receptor [26]. On the other hand, fibronectin, a glycoprotein involved in tissue remodeling, can be released in response to a variety of cytokines including TGF-β as its strongest stimulator. Therefore, by inhibiting the TGF-β-induced fibronectin production, NAC can be effective in blocking tissue remodeling [27]. To the best of our selleck kinase inhibitor knowledge, this is the first study evaluating the effect of NAC on TNF-α and TGF-β levels in human subjects with

AMI to investigate whether NAC might be beneficial in reducing remodeling. 2 Methods This randomized double-blind clinical trial (registration no.: IRCT201102283449N5 at http://​www.​irct.​ir) was conducted at the Tehran Heart Centre, Protein tyrosine phosphatase one of the referral teaching hospitals for cardiovascular disorders in Tehran, Iran from August 2010 to August 2011. The sample size of the study (44 patients in each group) was calculated based on the change in the serum TNF-α concentration following NAC administration [11]. The power of the study was considered to be 95 % (α = 0.05 and β = 0.20). After obtaining written informed consent, patients fulfilling diagnostic criteria for ST-segment elevation myocardial infarction (STEMI) were included in the study.