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Thus, azelaic acid and finasteride presumably induce NO-mediated angiogenesis in the flap tissue and improve survival flap. It is well established that agents with angiogenic activity could improve the outcomes in I/R injury in most tissues [19]. We recommend future investigations for determining the potential role of angiogenesis in improved surgical flap survival mediated by 5��-reductase inhibitors, azelaic acid and finasteride. Figure 3 was taken from the skin flap of one of the rats of each group in which the distal part of the flaps in control and L-NAME-treated group demonstrated extended necrotic area compared to azelaic acid- or [http://en.wikipedia.org/wiki/TRIB1 TRIB1] finasteride-treated rats. The latter two groups also showed a limited flap necrosis in the margins of distal part. This result further confirms the NO-dependent protective effects [http://www.selleckchem.com/products/MK-2206.html MK-2206 cell line] of azelaic acid and finasteride treatment in surgical flaps. In control group, total content of NO metabolites was 14.6 �� 2.5 ��mol/l tissue homogenate (Fig. 4). Treatment with azelaic acid and finasteride increased nitrite plus nitrate concentrations to 22.5 �� 3.1 ��mol/l and 24.9 �� 3 ��mol/l homogenate, respectively (P [http://www.selleckchem.com/products/pci-32765.html click here] kidney [20, 21], skin [18] and retina [22], some others have reported its detrimental effects on skin [23] and kidney [24]. Fig. 3 The effect of different types of treatments on necrosis of distal parts of skin flap seven days after surgery. Figures include a sample from each group. (A) The complete necrosis of distal sections in control group, (B) limited necrosis of skin flap in ... Fig. 4 Concentration of NO metabolites in skin tissue homogenate prepared from the flap area. Data are represented as means �� standard error of mean (SEM) of each group. *P