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Articles by Bahar Tunctan
Total Records ( 2 ) for Bahar Tunctan
  Bahar Tunctan , Belma Korkmaz , Hatice Yyldyrym , Lulufer Tamer , Ugur Atik and C. Kemal Buharalyoglu
  Overproduction of reactive oxygen and nitrogen species leads to oxidative stress and decreased total antioxidant capacity, which is responsible for high mortality from several diseases such as endotoxic shock. Nitric oxide (NO) produced by inducible NO synthase (iNOS) during endotoxemia is the major cause of vascular hyporeactivity, hypotension and multiple organ failure. In this study, we investigated whether increased production of NO contributes to renal oxidative stress in endotoxemic rat. Saline (4 mL kg-1, i.p.), endotoxin (Escherichia coli lipopolysaccharide, O111:B4; 10 mg kg-1, i.p.) and/or selective iNOS inhibitor (1,3-PBIT; 10 mg kg-1, i.p.) were administered to conscious male Wistar rats and mean arterial blood pressure was recorded at 1, 2, 3 and 4 hr after injection. Nitrite and malondialdehyde (MDA) levels and myeloperoxidase (MPO) activity were measured in the sera and/or kidney homogenates at the end of the experiments. Administration of endotoxin caused hypotension associated with increased systemic and renal nitrite production. 1,3-PBIT prevented these effects of endotoxin at 1 hr after injection of endotoxin. Renal MPO activity was decreased by endotoxin which was not changed by 1,3-PBIT. Endotoxin caused a decrease in MDA levels in the renal tissue, which was prevented by 1,3-PBIT. These data suggest that overproduction of NO by iNOS during endotoxemia decreases renal oxidative stress and that inhibition of iNOS restores total renal antioxidant capacity.
  Bahar Tunctan , Sefika Pinar Kucukkavruk , Meryem Temiz-Resitoglu , Demet Sinem Guden , Ayse Nihal Sari , Seyhan Sahan-Firat , Mahesh Paudyal , John Russell Falck and Kafait Ullah Malik
  Background and Objective: Nucleotide binding domain and leucine-rich repeat protein 3 (NLRP3) is reported to be involved in the pathogenesis of numerous inflammatory diseases including Alzheimer disease, Parkinson disease, Prion disease and type 2 diabetes mellitus. Previous studies have demonstrated that a stable synthetic analog of 20-hydroxyeicosatetraenoic acid (20-HETE), N-(20-hydroxyeicosa-5[Z],14[Z]-dienoyl)glycine (5,14-HEDGE), prevents vascular hyporeactivity, hypotension, tachycardia, inflammation and mortality in a rodent model of septic shock. This study was aimed to assess effect of 5,14-HEDGE on the changes in NLRP3/apoptosis-associated speck-like protein containing a caspase activation and recruitment domain (ASC)/pro-caspase-1 inflammasome in lipopolysaccharide (LPS)-induced septic shock in rats. Methodology: Rats were injected with saline (4 mL kg–1) or LPS (10 mg kg–1) at time 0. Blood pressure and heart rate were measured using a tail-cuff device. 5,14-HEDGE (30 mg kg–1) was administered to rats 1 h after injection of saline or LPS. The rats were sacrificed 4 h after saline or LPS injection and kidney, heart, thoracic aorta and superior mesenteric artery were isolated for measurement of caspase-1/11 p20, NLRP3, ASC and β-actin proteins as well as interleukin-1β (IL-1β) levels. Data were analysed by one-way ANOVA followed by Student-Newman-Keuls test for multiple comparisons, Kruskal-Wallis test followed by Dunns test for multiple comparisons and Student's test or Mann-Whitney U tests when appropriate. Results: Blood pressure decreased by 33 mmHg and heart rate increased by 63 bpm in the LPS-treated rats. In the LPS-treated rats, tissue protein expression of caspase-1/11 p20, NLRP3 and ASC in addition to IL-1β levels were increased. The 5,14-HEDGE prevented the LPS-induced changes. Conclusion: These findings suggest that inhibition of renal, cardiac and vascular formation/activity of NLRP3/ASC/pro-caspase-1 inflammasome involves in the protective effect of 5,14-HEDGE on LPS-induced septic shock in rats.
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