Browsing by Author "Bozkurt, Ayse"

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Aquaporins: Potential Targets in Inflammatory Diseases
(Ataturk Univ, 2023) Bozkurt, Ayse; Halici, Hamza; Yayla, Muhammed
Inflammation involves a long chain of molecular reactions and cellular activity designed to repair tissue damaged by various causes. The inflammatory process and its complex mechanisms have recently become a focus of interest for many researchers. After the onset of inflammation, various adverse conditions that initiate the inflammatory response need to be addressed; however, failure to limit the inflammatory reaction may result in the damage or destruction of host cells. Therefore, inflammatory reactions play a role in many different diseases. Aquaporins (AQPs), commonly referred to as water channels, are protein channels responsible for forming pores in the membranes of biological cells. Their main function is to aid in the movement of water between cells. Aquaporins not only regulate transepithelial fluid transport across membranes but also play a role in regulating essential events crucial for the inflammatory response. Aquaporins have been shown in many studies to have important roles in inflammatory diseases. This clearly indicates that AQPs may be potential targets for inflammatory diseases. This review summarizes the research to date on the structure and function of AQPs and provides an update on the relationship between AQPs and various human inflammatory diseases.
Effect of Pde 5 Inhibitor-Avanafil on Renal Ischemia/Reperfusion Injury in Rats
(Galenos Publ House, 2023) Yuksel, Tugba Nurcan; Halici, Zekai; Kaya, Cihangir; Bozkurt, Ayse; Tavaci, Taha; Civelek, Maide Sena; Ozdemir, Bengul
Aim: Renal ischemia-reperfusion injury (RI/RI) damages many organs, especially the kidney. Phosphodiesterase (PDE) 5 inhibitors has antioxidant and anti-inflammatory effects. Avanafil (AVA) is a second-generation PDE 5 inhibitor with greater PDE isoform selectivity. The aim of this study is to investigate the effects of AVA on RI/RI in rats. Materials and Methods: Forty rats were randomly divided into five groups (n=8): Sham; AVA 10; RI/RI; RI/RI + 5 mg/kg AVA, and RI/RI + 10 mg/ kg AVA. RI/RI in rats was established by clamping renal artery. An acute surgical experiment was performed for the induction of renal ischemia for 45 min by renal artery clamping followed by reperfusion for 24 h. Kidney tissues were investigated biochemically [malondialdehyde (MDA) and glutathione (GSH) with ELISA], molecularly [relative quantification of IL-113, nuclear factor-kappa B (NF-KB), and tumor necrosis factor-alpha (TNF-a) mRNA gene expression with qRT-PCR], and histopathologically (staining with Harris hematoxylin and eosin Y). Results: AVA administration ameliorated disturbances in MDA and GSH levels caused by RI/RI. AVA treatment improved the increase in the mRNA expressions of IL-113, NF-KB, and TNF-a in kidney tissues induced ischemia/reperfusion injury. AVA administration ameliorated histopathologic injury in kidney tissues caused by renal ischemia reperfusion. Moreover, the values closest to those of the sham group were obtained by administering 10 Conclusion: AVA administration improved renal ischemia/reperfusion-induced tissue injury by alleviating oxidative stress and inflammatory cascades that could be important in ischemia-reperfusion injury. These findings may provide a mechanistic basis for using AVA to treat RI/RI.
Effect of Trimetazidine Against Ovarian Ischemia/Reperfusion Injury in Rat Model: a New Pathway: Jak2/Stat3
(Mashhad Univ Med Sciences, 2023) Yuksel, Tugba Nurcan; Halici, Zekai; Cadirci, Elif; Toktay, Erdem; Ozdemir, Bengul; Bozkurt, Ayse
Objective(s): Ovarian ischemia/reperfusion (I/R) is an extremely complex pathological problem that begins with oxygen deprivation, progresses to excessive free radical production, and intensifies inflammation. The JAK2/STAT3 signaling pathway is a multipurpose signaling transcript channel that plays a role in several biological functions. Trimetazidine (TMZ) is a cellular anti-ischemic agent. This study aims to investigate the effects of TMZ on ovarian I/R injury in rats. Materials and Methods: sixty four rats were divided into 8 groups at random: healthy(group1); healthy+TMZ20(group2); ischemia (I) (group 3); I+TMZ10(group4); I+ TMZ20(group5); I/R(group6); I/R+TMZ10(group7); I/R+TMZ20(group8). Vascular clamps were placed just beneath the ovaries and over the uterine horns for 3 hr to induce ischemia. The clamps were removed for the reperfusion groups, and the rats were reperfused with care to ensure that the blood flowed into the ovaries, subjecting them to reperfusion for 3 hr. TMZ was administered orally by gavage 6 and 1 hr before operations. At the end of the experiment, ovarian tissues were removed for biochemical, molecular, and histopathological investigation. Results: TMZ administration ameliorated ischemia/reperfusion-induced disturbances in GSH and MDA levels. TMZ treatment inhibited I/R-induced JAK2/STAT3 signaling pathway activation in ovarian tissues. TMZ administration also improved the increase in the mRNA expressions of IL1 beta, TNF-alpha, and NF-KB caused by ischemia/reperfusion injury. Moreover, TMZ treatment improved histopathologic injury in ovarian tissues caused by ischemia/reperfusion. Conclusion: TMZ treatment protected rats against ovarian ischemia/reperfusion injury by alleviating oxidative stress and inflammatory cascades. These findings may provide a mechanistic basis for using TMZ to treat ovarian ischemia-reperfusion injury.
Investigation of Antiepileptic Potentials of Usnic Acid and Some Lichen Species on the Behavioral and Biochemical Levels in Pentylenetetrazole-Induced Kindling Model of Epilepsy
(Marmara Univ, 2024) Berkoz, Mehmet; Yunusoglu, Oruc; Aslan, Ali; Bozkurt, Ayse
In this study, the effects of various lichen and usnic acid applications on seizure scores and biochemical parameters in brain tissue in rats with epilepsy model was investigated. For this aim, 91 rats were divided into 13 groups, each containing 7 rats, which were: control, pentylenetetrazole (PTZ) (35 mg/kg), PTZ + Valproic acid (100 mg/kg), PTZ + Dolichousnea longissima(200 mg/kg), PTZ + Dolichousnea longissima (400 mg/kg), PTZ + Xanthoparmelia somloensis( 50 mg/kg), PTZ + Xanthoparmelia somloensis(200 mg/kg), PTZ + Cetraria islandica(250 mg/kg), PTZ + Cetraria islandica(500 mg/kg), PTZ + Pseudevernia furfuracea(250 mg/kg), PTZ + Pseudevernia furfuracea(500 mg/kg), PTZ + usnic acid (50 mg/kg), and PTZ + usnic acid (200 mg/kg). All items were applied with an interval of 120 minutes for a period of one week. Seizure detection, seizure scores and total seizure duration of each group was recorded. After the applications, oxidative stress parameters and acetylcholinesterase enzyme activity in the brain tissue of rats were measured. There was no difference between the groups in the 1st, 2nd, and 3rdinjections (p>0.05). Starting from the 4th injection, the seizure score was significantly higher in the PTZ group compared to the control group (p<0.05). When the effects on locomotor activity were evaluated, no difference was found between any group (p>0.05). In PTZ applied groups, an increase in lipid and protein oxidation as well as a decrease in antioxidant and acetylcholine esterase levels were observed(p<0.05). Valproic acid, high concentration of lichen extract applications and high and low concentration of usnic acid applications were found to reverse this situation (p<0.05). As a result, various lichen extracts and usnic acid were shown to reduce behavioral symptoms and oxidative stress of epilepsy, with a preventive effect on the complications of epilepsy.
Protective Effects of Ace/Nep Dual Inhibitor Omapatrilat for Indomethacin-Induced Gastric Ulcer
(Galenos Publ House, 2023) Erkayman, Kadir Giray; Ugan, Ruestem Anil; Magden, Zeynep Berna Aksakkalı; Yilmaz, Eda; Bozkurt, Ayse; Cadirci, Elif
Aim: The renin-angiotensin-aldosterone system (RAAS) plays important roles in oxidative stress and various gastroenterological mechanisms. Omapatrilat, an RAAS-acting agent, inhibits both neprilysin neutral endopeptidase (NEP) and angiotensin converting enzyme (ACE) and may therefore affect protective mechanisms against gastric ulcer. Therefore, this study examined the gastroprotective role of omapatrilat in a mouse model of gastric ulcer induced by indomethacin to reveal pharmacological and biochemical changes resulting from omapatrilat treatment. Materials and Methods: Forty-two BALB/c mice were divided into seven groups: control, 40 mg/kg omapatrilat only, 25 mg/kg indomethacin only, indomethacin and 40 mg/kg famotidine, and three groups with indomethacin and 10-40 mg/kg omapatrilat. All chemicals were administered by oral gavage in 0.5 mL of 0.9% NaCl solution at the determined doses. Stomach ulcers were induced by indomethacin in mice treated with famotidine (40 mg/kg) and omapatrilat (10-40 mg/kg). Stomach tissue samples were examined macroscopically. Oxidative stress biomarkers of malondialdehyde (MDA), glutathione (GSH), NEP and ACE levels as well as superoxide dismutase (SOD) activity were measured. Results: The best antiulcer activity was measured with 40 mg/kg omapatrilat, where the gastric damage observed in the ulcer groups was significantly reversed, and gave the most similar results to the specific famotidine treatment. In relation with the increasing omapatrilat dose, SOD activity was corrected as well as GSH and MDA levels. Also the levels of ACE and NEP decreased back towards those measured in the control group. Therefore, these macroscopic and biochemical findings indicating reversal of gastrotoxicity and gastric ulcer indications demonstrate the role of omapatrilat's NEP and ACE inhibition in indomethacin toxicity, and its strong gastroprotective potential. Conclusion: Dual inhibition of NEP and ACE by omapatrilat may suppress oxidative stress associated with indomethacin-induced gastric ulcer. Therefore, the protective effect of omapatrilat in the treatment of ulcers may lead to the search for new treatment strategies.
Targeting Aquaporin-5 by Phosphodiesterase 4 Inhibition Offers New Therapeutic Opportunities for Ovarian Ischemia Reperfusion Injury in Rats
(Springer Heidelberg, 2024) Bozkurt, Ayse; Karakoy, Zeynep; Aydin, Pelin; Ozdemir, Bengul; Toktay, Erdem; Halici, Zekai; Cadirci, Elif
This study aimed to examine the effect of Phosphodiesterase 4 (PDE4) inhibition on Aquaporin-5 (AQP5) and its potential cell signaling pathway in the ovarian ischemia reperfusion (OIR) model. Thirty adult female rats were divided into five groups: Group 1; Control: Sham operation, Group 2; OIR that 3 hour ischemia followed by 3 hour reperfusion, Group 3; OIR + Rolipram 1 mg/kg, Group 4; OIR + Rolipram 3 mg/kg, Group 5; OIR + Rolipram 5 mg/kg. Rolipram was administered intraperitoneally to the rats in groups 3-4 and 5 at determined doses 30 minutes before reperfusion. From ovary tissue; Tumor necrosis factor-a (TNF-alpha), Cyclic adenosine monophosphate (cAMP), Nuclear factor kappa (NF-kappa B), Interleukin-6 (IL-6), Phosphodiesterase 4D (PDE4D), Mitogen-activated protein kinase (MAPK) and AQP5 levels were measured by ELISA. We also measured the level of AQP5 in ovary tissue by real-time reverse-transcription polymerase chain reaction (RT-PCR). In the OIR groups; TNF-alpha, NF-kappa B, IL-6, MAPK inflammatory levels increased, and cAMP and AQP5 levels decreased, which improved with the administration of rolipram doses. Also histopathological results showed damaged ovarian tissue after OIR, while rolipram administration decrased tissue damage in a dose dependent manner. We propose that the protective effect of PDE4 inhibition in OIR may be regulated by AQP5 and its potential cell signaling pathway and may be a new target in OIR therapy. However, clinical studies are needed to appraise these data in humans.