Person: ÜSTÜNOVA, SAVAŞ
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Publication Metadata only GÜNCEL FARMAKOLOJİ Fizyoloji Temelinde Hasta Odaklı Yaklaşım(2022-09-01T00:00:00Z) Üstünova, Savaş; ÜSTÜNOVA, SAVAŞPublication Metadata only The Effect of Theobroma Cacao on Hyperlipidemic Rats(2019-03-14) Kılıç A.; Üstünova S.; KILIÇ, AYSU; ÜSTÜNOVA, SAVAŞPublication Metadata only FİZYOLOJİ(2019-02-01) MERAL, İSMAİL; ÜSTÜNOVA, SAVAŞ; MERAL, İSMAİL; ÜSTÜNOVA, SAVAŞPublication Metadata only Effects of Angiotensin IV on Learning-Memory and Hippocampal Oxidative Stress in Diabetic Rats(2019-12-01T00:00:00Z) KILIÇ, Aysu; ÜSTÜNOVA, SAVAŞ; ELİBOL, BİRSEN; Bulut, Huri; MERAL, İSMAİL; Sahin, Emine Gulderen; KILIÇ, AYSU; ÜSTÜNOVA, SAVAŞ; ELİBOL, BİRSEN; BULUT, HURI; MERAL, İSMAİLPublication Metadata only The Protective Effect of Cinnamomum Zeylanicum in Streptozotocin-Induced Diabetic Rats(2019-03-29) Kılıç A.; Üstünova S.; KILIÇ, AYSU; ÜSTÜNOVA, SAVAŞPublication Metadata only Role of Angiotensin TYpe I and II receptor Blockade in Ischemia/Reperfusion Injury of Isolated Rat Heart(2017-05-04) Kılıç, AYSU; ÜSTÜNOVA, SAVAŞ; Usta, Cansu; BULUT, HURİ; ÜYÜKLÜ, MEHMET; Demirci-Tansel, Cihan; MERAL, İSMAİL; Artumak, Elif; Gurevin-Gürel, Ebru; KILIÇ, AYSU; ÜSTÜNOVA, SAVAŞ; BULUT, HURI; ÜYÜKLÜ, MEHMET; MERAL, İSMAİLPublication Metadata only Role of ischemic preconditioning and tempol in ischemia/reperfusion injury in isolated rat heart(2013-07-01T00:00:00Z) Erol, D.; Ustunova, SAVAŞ; Gurel, E.; Dedeakayogullari, H.; Demirci-Tansel, C.; ÜSTÜNOVA, SAVAŞPublication Metadata only Hexokinase cellular trafficking in ischemia-reperfusion and ischemic preconditioning is altered in type I diabetic heart(2013-07-01T00:00:00Z) Gurel, Ebru; Ustunova, SAVAŞ; Kapucu, Aysegul; Yilmazer, Nadim; EERBEEK, Otto; NEDERLOF, Rianne; HOLLMANN, Markus W.; Demirci-Tansel, Cihan; ZUURBIER, Coert J.; ÜSTÜNOVA, SAVAŞDiabetes mellitus (DM) has been reported to alter the cardiac response to ischemia-reperfusion (IR). In addition, cardioprotection induced by ischemic preconditioning (IPC) is often impaired in diabetes. We have previously shown that the subcellular localisation of the glycolytic enzyme hexokinase (HK) is causally related to IR injury and IPC protective potential. Especially the binding of HK to mitochondria and prevention of HK solubilisation (HK detachment from mitochondria) during ischemia confers cardioprotection. It is unknown whether diabetes affects HK localisation during IR and IPC as compared to non-diabetes. In this study we hypothesize that DM alters cellular trafficking of hexokinase in response to IR and IPC, possibly explaining the altered response to IR and IPC in diabetic heart. Control (CON) and type I diabetic (DM) rat hearts (65 mg/kg streptozotocin, 4 weeks) were isolated and perfused in Langendorff-mode and subjected to 35 min I and 30 min R with or without IPC (3 times 5 min I). Cytosolic and mitochondrial fractions were obtained at (1) baseline, i.e. after IPC but before I, (2) 35 min I, (3) 5 min R and (4) 30 min R. DM improved rate-pressure product recovery (RPP; 71 +/- A 10 % baseline (DM) versus 9 +/- A 1 % baseline (CON) and decreased contracture (end-diastolic pressure: 24 +/- A 8 mmHg (DM) vs 77 +/- A 4 mmHg (CON)) after IR as compared to control, and was associated with prevention of HK solubilisation at 35 min I. IPC improved cardiac function in CON but not in DM hearts. IPC in CON prevented HK solubilisation at 35 min I and at 5 min R, with a trend for increased mitochondrial HK. In contrast, the non-effective IPC in DM was associated with solubilisation of HK and decreased mitochondrial HK at early reperfusion and a reciprocal behaviour at late reperfusion. We conclude that type I DM significantly altered cellular HK translocation patterns in the heart in response to IR and IPC, possibly explaining altered response to IR and IPC in diabetes.Publication Open Access Effects of Cichorium Intybus on GABAA Receptors and Apoptosis in Pentyleneterazole-PTZ Kindling in Rats.(2021-08-01T00:00:00Z) Meral, İsmail; Eşrefoğlu, Mukaddes; Kara, Mehmet; Erkeç, Özlem Ergül; Tok, Olgu Enis; Armağan, Metin; MERAL, İSMAİL; EŞREFOĞLU, MUKADDES; ÜSTÜNOVA, SAVAŞPublication Open Access Hydrogen Sulphide and Nitric Oxide Cooperate in Cardioprotection Against Ischemia/Reperfusion Injury in Isolated Rat Heart(2020-09-01T00:00:00Z) ÜSTÜNOVA, SAVAŞ; TAKIR, SELÇUK; YILMAZER, NADİM; Bulut, Huri; ALTINDİREK, Didem; HATIRNAZ NG, Özden; Tansel, Cihan Demirci; Dogan, B. Sonmez Uydes; ÖZBEK, Uğur; ARMUTAK, Elif İlkay; Gurevin, Ebru Gurel; ÜSTÜNOVA, SAVAŞBackground/Aim: This study was designed to provide further evidence for the interactions between hydrogen sulfide (H2S) and nitric oxide (NO) in ischemia/reperfiision (I/R) injury. Materials and Methods: Rat hearts were studied with the Langendorff technique using the H2S donor sodium hydrosulfide (NaHS, 40 mu M) and the cystathionine gamma-lyase (CTH or CSE) inhibitor DL-propargylglycine (PAG, 1 mM). NO synthase inhibitor L-NG-nitroarginine methyl ester (L-NAME, 30 mg/kg, 7 days) was administered before the isolation. The hearts were homogenized for biochemical and molecular analysis. Results: NaHS reversed I/R-induced cardiac performance impairment, increased tissue nitric oxide production and decreased tissue markers for cardiac injury, while L-NAME inhibited these effects. The expression of CTH was increased with PAG, which was suppressed by L-NAME. Conclusion: H2S and NO increase each other-s production suggesting their interaction and cooperation in cardioprotection against I/R injury.