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    Evaluation of immunohistochemical expression of GSTA1 and GSTP1 isoenzymes before and after treatment of Trx and L-NAME in experimental hepatic ischemia/reperfusion model
    (Society of Pharmaceutical Sciences of Ankara (FABAD), 2012) Güler Şimşek G.; Kiliç M.; Oğuz?üzun S.; Karahan S.; Akin O.K.; Kiliç N.; Serdar M.A.
    Ischemia/reperfusion (I/R) causes formation of Reactive Oxygen Species (ROS) in tissues, in response to which injured cells improve a number of defense mechanisms including Glutathione S-Transferases (GSTs). The aim of this study was to investigate the expressions of GSTA1 and GSTP1 following Thioredoxin (Trx) and N-nitro-L-arginine methyl ester (L-NAME) treatment in a rat model of hepatic I/R model. A total of 50 Wistar rats were randomly allocated into 5 groups: sham (n = 10), control (I/R) (n = 10), Trx (n = 10), L-NAME (n = 10), and Trx+L-NAME (n = 10). With an exception to those in sham group, all rats were subjected to a hepatic ischemia process for an hour and then subsequent reperfusion. GSTA1 and GSTP1 expressions in the liver tissues were determined by immunohistochemical method. The GSTA1 expression was absent in sham group while varying degrees of expression occurred in other groups. The GSTA1 expression was significantly higher in Trx/L-NAME group compared to other groups (p <0.05). GSTP1 expression was no difference between groups (p >0.05). As a result, we think that GSTA1 expression may have increased in response to I/R as a part of the liver oxygen radical scavenging process.
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    Protein profiling of anastomosed facial nerve treated with mesenchymal stromal cells
    (Elsevier Inc., 2012) Satar B.; Hidir Y.; Serdar M.A.; Kucuktag Z.; Ural A.U.; Avcu F.; Safali M.
    Background aims. The types of proteins released from mesenchymal stromal cells (MSC) are still unclear. Our aim was to compare apoptosis scores and the expression of myelin-associated glycoprotein (MAG), myelin basic protein (MBP), neural cell adhesion molecule (NCAM)-1,matrix metalloproteinase (MMP)-1A, tissue inhibitor of metalloproteinase (TIMP)-1, TIMP-1/MMP-1A ratio, nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), ciliary neurotrophic factor (CNTF), neurotrophin (NT)-3, NT-4, glial cell-derived neurotropic factor (GDNF), leukemia inhibitory factor (LIF), basic fibroblast growth factor (FGF)-2, insulin-like growth factor (IGF)-1, platelet-derived growth factor (PDGF)-? and transforming growth factor (TGF)-?1 in anastomosed facial nerves that had been treated with or without MSC. Methods. In seven rats, the buccal branch of the right facial nerve was transected, anastomosed and treated with MSC (anastomosed + MSC group). The left buccal branch was anastomosed only (anastomosed-only group). The left mandibular branch served as an intact nerve group. On days 1820, the distal segments of the branches were examined in terms of expression of the mentioned proteins and apoptosis scores using polymerase chain reaction (PCR) and terminal deoxynucleotidyl transferase-mediated digoxigenin-UTP nick end labeling (TUNEL) assays. Results. MSC application significantly increased CNTF, PDGF-?, LIF, TGF-?1, BDNF and NT-3 expression (P < 0.05). MAG expression slightly decreased whereas NCAM-1, MMP-1A and FGF-2 slightly increased(P > 0.05). Changes in other proteins and apoptosis scores were not significant. Conclusions. These results suggest that MSC increases expression of CNTF, PDGF-?, LIF,TGF-?1, BDNF and NT-3. MAG, NCAM-1, MMP-1A and FGF-2 expressions were slightly changed in this stage of nerve regeneration. The comparison of apoptotic activity was not conclusive. Overall, it appears that MSC might have differential effects on the mentioned tissue-related proteins and trophic/growth factors. © 2012 Informa Healthcare.