The results indicated that exogenous supply of Sema 3A enhances p53 phosphorylation at Ser-15 residue

een well recognized and widely performed to prevent the CIN, the incidence of CIN did not decrease. So the efficacy of many other interventions are still under GW 501516 web testing. From 2004 to 2011, a few studies focused on using statin as a specific prophylactic measure of CIN prevention have been published. In this meta-analysis of 7 randomized controlled trials, we found that statin could significantly reduce the risk of CIN without decreasing the incidence of death or need for dialysis. However, there was marked clinical heterogeneity among these studies, indicating the need ” for a large definitive RCT. In addition to their intended impact on blood cholesterol levels, statins have been found to have multiple nonlipid-lowering effects, which include enhancement of endothelial nitric oxide production, anti-inflammatory and “8549627 antioxidative actions. Given their pleiotropic effects, statins could decrease acute renal injury after iodinated contrast administration through two major pathways. Firstly, statins may modulate the kidney hypoperfusion after contrast administration by downregulation of angiotensin receptors and decreased synthesis of endothelin-1. Secondly, toxic damage on the tubular cells by oxygen-free radicals and proinflammatory cytokines may be decreased by antiinflammatory effects of statins that inhibit tissue factor expression by macrophages and prevent the activation of nuclear factor-kB. Moreover, its nonlipid-lowering effect could be demonstrated within a few hours after statin therapy initiation. Although many clinical trials have shown that high-dose statins provide more clinical benefits, such as atorvastatin 80 mg can further reduce vascular risks compared with low-dose statin therapy, the threshold of statins to reduce the risks of CIN remains unknown. In this meta-analysis, all of the included trials were short-term high-dose statin therapy, two of which compared two different doses of statin in preventing CIN. We found that high-dose statin therapy significantly lowered the incident of CIN compared with low-dose statin therapy. These results were consistent with the previous studies that high-dose statin has been shown to be more potent to suppress platelet activity and inflammatory chemokines than low-dose statin therapy. The results of this meta-analysis are not in line with research from Zhang T et al, Zhang L et al and Pappy R et al which showed non-statistically significant reduction in the incidence of CIN with statin treatment from the pooled estimate for the randomized trials. In fact, Zhang T et al and Pappy R et al included both randomized and non-randomized trials in their meta-analysis, while the latter might lead to potential bias because it was impossible to completely remove interference of unknown confounding factors. The meta-analysis by Zhang L et al involved only 4 RCTs, which included an abstract that overlapped with participants included in a separate study by the same author. Therefore, to avoid including any individual participant more than once, abstract by the same author was excluded in our meta-analysis. Moreover, all of above three meta-analysis did not include two large scale studies published in recent days. Although the main conclusion in our meta-analysis was similar to that in the recent meta-analysis, these similar results shall be treated with cautious interpretation. First, in our metaanalysis, we found that statin was able to prevent CIN only in studies with lower quality, especially tho