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by
Bahar Tunctan |
Total Records (
2 ) for
Bahar Tunctan |
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Bahar Tunctan
,
Belma Korkmaz
,
Hatice Yyldyrym
,
Lulufer Tamer
,
Ugur Atik
and
C. Kemal Buharalyoglu
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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. |
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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
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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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