Despite all contemporary surgical techniques pores and skin flap that’s considered as the primary method generally in most reconstructive surgeries puts your skin cells at threat of necrosis and apoptosis produced from ischemia. part for finasteride and azelaic acidity in conserving the flap following the ischemia reperfusion insult. Key Phrases: Azelaic acid Apoptosis Finasteride Skin flaps Introduction Skin flap is considered as the main method in most reconstructive surgeries (1) and its application in providing suitable tissue coverage has an essential role in increasing the patients’ life quality (2). Despite the rapid progresses in skin flap application in clinic ischemia may restrict its SGX-523 utility (3). The phenomenon of ischemia-reperfusion (IR) has been postulated to be an important DKK4 event in skin flap surgery which leads to major complications and loss of tissue (4) but also involves in other chronic wounds such as venous stasis and diabetic foot ulcers (5-6). Therefore finding the treatments which reduce flap injury would be highly advantageous in reconstructive surgery. Oxidative stress derived from IR injury through producing the reactive oxygen species (ROS) and oxidative damage causes DNA modification lipid peroxidation and secretion of inflammatory cytokines (7-8). In addition apoptosis is induced with ischemic insults in skin tissue (8). Plenty of proteins and number of genes regulate the apoptosis in which two pairs of proteins are more important (including BCL-2 and Bax). BCL-2 family of proteins is found in external surface of mitochondria and divided to 3 groups including: antiapoptotic SGX-523 proteins like BCL-2 and BclxL proapoptotic proteins like Bax and BAD and the proteins with apoptotic activity like Bik (9-11). After occurring a severe damage in the DNA of cells in a way that cannot be repaired it will undergo the apoptosis in which activation of p53 causes Bax (BCL-2 associated x-protein). Bax protein exists in the external membrane of mitochondria with some other proteins making the complex of Apoptosome which has the key role in activating the caspases and inducting the apoptosis (12-13). Yet it has been shown that various pharmacological agents including inducible nitric oxide synthase (iNOS) (14) botulinum toxin A (15) Hemoglobin vesicles (16) Erythropoitin (17) University of Wisconsin solution (18) and Enalapril (19) protects against the ischemia-induced injury of skin flaps. In present study we evaluated the effects of two different drugs finasteride and Azelaic acid on BCL-2 and bax expression after the skin ischemia reperfusion. Experimental This experiment received the approval of ethical committee of the Center for Research and Training in Skin Disease and Leprosy Tehran University of Medical Sciences. Twenty-one Sprauge-Dawley male rats (200-250 g) were chosen for random pattern cranial-based pores and skin flap elevation (19). The rats had been split into 3 sets of 7 rats including one control and two treatment organizations in flap cells which the proteins expression was examined through getting different pharmacologic real estate agents for SGX-523 preconditioning the flaps. Almost all along the scholarly research period the rats were located in solitary cages given ample food and water. Preoperative arrangements included shaving administrating (ROS) and oxidative harm causes DNA changes lipid peroxidation and secretion of inflammatory cytokines (7-8). Furthermore apoptosis can be induced with ischemic insults in pores and skin cells (8). A lot of proteins and amount of genes regulate the apoptosis where two pairs of proteins are even more essential (including BCL-2 and Bax). SGX-523 BCL-2 category of protein is situated in exterior surface area of mitochondria and divided to 3 organizations including: antiapoptotic SGX-523 protein like BCL-2 and BclxL proapoptotic protein like Bax and Poor and the protein with apoptotic activity like Bik (9-11). After happening a severe harm in the DNA of cells in a manner that cannot be fixed it will go through the apoptosis where activation of p53 causes Bax (BCL-2 connected x-protein). Bax proteins is present in the exterior membrane of mitochondria with various other proteins producing the complicated of Apoptosome which includes the key part in activating the caspases and inducting the apoptosis (12-13). However it’s been demonstrated that different pharmacological real estate agents including inducible nitric oxide synthase (iNOS) (14) botulinum toxin A (15) Hemoglobin vesicles (16) Erythropoitin (17) College or university of Wisconsin remedy (18) and Enalapril (19) shields against the ischemia-induced damage of pores and skin flaps. In present research we evaluated the consequences of two different medicines.