Antagonism of TGF-β can lead to two opposite effects depending on the time. Early TGF-β inhibition, MAPK inhibitor within the first 24 h

after AMI, can increase levels of pro-inflammatory cytokines and infiltration of neutrophils, and consequently intensify the expression of MMPs which may result in aggravation of LV dysfunction and increase the rate of mortality [8]. Conversely, TGF-β antagonism after this time can have beneficial effects by reducing the extent of fibrotic and hypertrophic changes in the myocardium [9, 29, 30]. In the present study, we found that NAC did not have any significant effect on the level of TGF-β at 24 h, the time at which its inhibition can have a detrimental outcome. However, NAC administration could prevent TGF-β from increasing at 72 h as compared with patients receiving placebo, the time at which the proliferative

phase of remodeling will start, and therefore its suppression could have favorable therapeutic effects. Higher serum concentrations of TGF-β had strong positive correlations with LV systolic function and patients’ ejection fraction in the present study, which showed that a relationship existed between TGF-β and cardiac check details remodeling. This finding puts more emphasis on the necessity of TGF-β inhibition to prevent cardiac remodeling and its untoward consequences. As TGF-β was shown to promote extracellular matrix synthesis and collagen crosslink took place after MI, it could have an important role in the signaling AP26113 order pathway of LV remodeling [31]. An increased TGF-β level after MI was associated

with the development of heart failure secondary to cardiac remodeling [31]. In the present study, a significant association was found between serum concentrations of TGF-β and the presence of diabetes. This finding is in line with a previous study, which showed a relationship between elevated serum concentrations of TGF-β and diabetes after considering demographic, Gefitinib mw anthropometric, metabolic, and lifestyle factors [32]. This could be explained by the mechanism of insulin resistance as inflammation can be an important factor in its development and thus the incidence of diabetes [33]. Another association was between a history of statin use and the level of TGF-β. TGF-β is one of the most important mediators of cardiomyocyte fibrosis and hypertrophic growth through the action of Smad proteins as an essential component of the intracellular signaling pathway [34]. Statins can suppress the up-regulation of TGF-β induced by angiotensin and the resultant cardiac remodeling and systolic dysfunction [35, 36]. This suppression can be attributed to the inhibition of superoxide production favored by angiotensin [36]. Thus, the low level of TGF-β in patients receiving statins as observed in the present study is a reasonable finding. The other finding of this study was the relationship between the coronary angiography finding, in particular stenosis of the LMCA, and TGF-β levels.