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Öğe The effect of dietary supplementation with n-3 polyunsaturated fatty acids on the generation of platelet-activating factor and leukotriene B4 in hypoxic-ischemic brain in young mice(Churchill Livingstone, 2002) Akisu M.; Huseyinov A.; Baka M.; Yalaz M.; Kultursay N.Platelet-activating factor (PAF), leukotriene B4 (LTB4) and other cytokines have been indicated to be responsible for the neuronal damage in hypoxic-ischemic brain. Diets in omega-3 (n-3) fatty acids appear to have an antiinflammatory effect, which is thought to be due to decrease in active prostaglandins and leukotrienes production after incorporation of these fatty acids into cell membrane phospholipids. We investigated the effect of dietary supplementation with n-3 fatty acids on endogenous PAF and LTB4 biosynthesis in hypoxic-ischemic brain of young mice. Young mice were randomly divided into four groups: Group 1 mice were fed standard chow (n-3 polyunsaturated fatty acids free); Group 2 and Group 3 mice were given standard diet supplemented with 10% by weight of fish oil, as source of n-3 polyunsaturated fatty acids, for 3 and 6 weeks, respectively. Group 4 mice served as control. We injured the right cerebral hemisphere of young mice by ligating the right common carotid artery and exposing the mice to 8% oxygen for 60 min. Approximately 10-fold increase in PAF concentration was determined in hypoxic-ischemic brain tissue of Group 1 mice. Tissue concentration of PAF showed a profound decline in Group 3 mice compared to Groups 1 and 2 (P<0.01, P<0.05, respectively). LTB4 was also significantly elevated in the brain of Group 1 mice when compared to the brain of control mice (P<0.001). A striking decline was observed in the concentration of LTB4 in both Group 2 and Group 3 mice compared to Group 1 mice (P<0.05, P<0.01, respectively). The present study shows that n-3 fatty-acid-enriched diet inhibits endogenous PAF and LTB4 generation in hypoxic-ischemic brain tissue; however it demonstrates that 6 weeks of dietary supplementation with n-3 fatty acids results in a significant decrease in tissue level of PAF in the brain. © 2002 Elsevier Science Ltd. All rights reserved.Öğe Effect of fish-oil enriched diet on leukotriene level in experimental trinitrobenzen sulfonic acid (TNB) colitis in rats [Deneysel trinitrobenzensulfonik asit (TNB) kolitinde balik yagindan zengin diyetin lokotrien duzeylerine etkisi](1997) Yuceyar H.; Ozutemiz O.; Huseyinov A.; Alkanat M.; Bor S.; Coker I.; Batur Y.The etiology of inflammatory bowel disease (IBD) is still unknown and the treatment of recurrences of IBD is also inadequate. In this study, we investigated the protective role of a fish oil (FO) - enriched diet in a rat model of TNP colitis. 20 male Wistar-Albino rats were randomized into 2 groups (n = 10). All of them were fed for 6 weeks with a standard diet (group-1) and standard diet plus FO (% 8) (group-2). At the end of this period, TNP (30 mg in 0,25 ml of % 30 ethanol) were intrarectally administered. After two weeks, the rats were sacrificed and the distal colon was removed. The Specimens were histopathologically evaluated. The MPO enzyme activities were measured and leukotriene B4 (LTB4) and LTC4 levels were determined by radioimmunoassay. MPO activities, LTB4 and LTC4 levels were (respectively) 30,41 ± 1,94 Ug/wet weight, 372,1 ± 65,24 pg/mg tissue protein, 450,0 ± 56,45 pg/mg tissue protein. These levels were reduced in group-2 (respectively) 2,43 ± 0,47 Ug/wet weight, 34,5 ± 8,16 and 64,0 ± 10,46 pg/mg tissue protein. There were significant differences in MPO activities, LTB4 and LTC4 levels and histopathological scores between the two groups (respectively p = 0,0108, p = 0,0034, p = 0,0024, p = 0,002). In conclusion, FO-enriched diet could reduce the colon damage in TNP colitis in rats.Öğe Effect of nedocromil sodium on invivo and invitro secretion of lipid mediators from peripheral leukocytes of asthmatic children(1997) Huseyinov A.; Yuksel H.; Tanac R.; Demir E.; Coker I.[No abstract available]Öğe Effects of selective cyclooxygenase-2 inhibition on gingival tissue levels of prostaglandin E2 and prostaglandin F2? and clinical parameters of chronic periodontitis(2003) Vardar S.; Baylas H.; Huseyinov A.Background: The purpose of the present study was to evaluate the effect of a relatively selective cyclooxygenase (COX)-2 inhibitor (nimesulide) and non-selective COX-1/COX-2 inhibitor (naproxen) used as an adjunct to non-surgical (scaling and root planing [SRP]) periodontal therapy in chronic periodontitis patients on the gingival tissue (GT) levels of prostaglandin (PG)E2 and PGF2?. Methods: Thirty patients with chronic periodontitis were divided into 3 groups of 10 each. One group received 100 mg of nimesulide; one received 275 mg of naproxen sodium; and the third group received placebo tablets in a 2 _xt 1 regimen for 10 days as an adjunct to SRP. GT samples were obtained before drug intake and on day 10. Plaque index (PI) and papillary bleeding index (PBI) scores were recorded at baseline, day 10, and at 3 months; probing depth (PD) and clinical attachment level (CAL) were recorded at baseline and at 3 months. The levels of PGE2 were detected using an enzyme immunoassay (EIA), and the levels of PGF2? were analyzed by radioimmunoassay (RIA). Differences among and within the groups were assessed using non-parametric statistical analysis. Ten periodontally healthy individuals served as controls. Results: All 3 groups showed statistically significant reductions in PBI and PI on day 10 and at 3 months (P <0.02), and in PD and CAL at 3 months (P <0.02, P <0.05, respectively). In the naproxen group, GT PGE2 levels exhibited a significant decrease (P <0.05). However, the decrease of GT PGE2 levels in the nimesulide group was insignificant (P >0.05), while a significant increase was observed in the placebo group (P <0.05) on day 10. Both the nimesulide and naproxen groups showed a significant decrease (P <0.05) in PGF2? level, while the placebo group showed a significant increase (P <0.05). Conclusions: Nimesulides, relatively selective COX-2 inhibitors, may have additional inhibitory effects on GT PGF2? levels in the first week following non-surgical periodontal treatment. However, nimesulide has an insignificant effect on reducing PGE2 levels in gingival tissue. The determination of GT levels of COX-1 and COX-2 enzymes as well as PGE2 and PGF2? in long-term studies may provide further support for the adjunctive use of selective COX-2 inhibitors in treatment of chronic periodontitis.Öğe Leukotrienes in cerulein-induced acute pancreatitis in rats and effect of octreotide(1999) Ersoz G.; Huseyinov A.; Ozutemiz O.; Yuce G.; Coker I.; Batur Y.The role of leukotrienes (LTs) in inflammation, which is widespread in some diseases, suggests that LTs may play an important role in the pathophysiology of acute pancreatitis (AP). The aim of this study was to investigate the levels of LT in the liver, pancreatic tissue and plasma of rats with cerulein-induced acute pancreatitis and the effect of octreotide on these levels. Methods: Thirty three Wistar Albino rats (170-220g) were included in the study, and randomly allocated to 5 groups (n=6-7) which were given: A-Control, BI: four successive doses of cerulein, 20 µg/kg SC at one hourly intervals. BII: Same as group CI, with addition of four successive doses of octreoide, 5 µg/kg at one hourly intervals. CI: Same as group BI with the addition of saline given every 12 hr for 1 wk CII-Same as group IV, but with 5 µg/kg octreotide given instead of saline. LTs were measured by RAI method. Results: these were expressed as (mean±SEM) pg/mg tissue protein for liver and pancreas and pg/ml for plasma. Plasma, pancreas and liver LTB4 levels were: 15.48±4.03, 13.51±2.99 and 33.42±6.01 in group A; 32.44±2.89, 32.71±3.24 and 37.42±2.29 in group BI; 18.21±2.67, 6.78±1.69 and 23.42±3.56 in group BII; 26.03±2.53, 96.66±13.22 and 38.50±5.69 in group CI; 20.0±1.75, 61.5±2.14 and 27.83±1.35 in group CII respectively. Plasma, pancreas and liver LTC4 levels were found 20.71±6.99, 22.57±6.76 and 11.14±5.44 in group A; 31.85±3.37, 51.14±13.92 and 21.14±4.29 in group BI; 10.14±2.91, 31.57±10.11, 13.14±2.65 in group BII; 29.00±3.69, 84.00±17.47 and 30.83±2.42 in group CI and 19.16±1.90, 59.66±11.72 and 9.83±4.50 in group CII respectively. Plasma LTB4 levels were significantly different between group A and group BI (p<0.01), pancreatic LTB4 levels were significantly different between group A: and groups BI, CI and CII (p<0.01), group BII plasma LTC4 levels was significantly lower then group BI (p<0.01) and pancreas and liver LTC4 levels were significantly different between groups A and CI (p<0.05). Conclusion: In the acute phase of acute pancreatitis, LTB4 levels increase in plasma and pancreatic tissue. Octreotide decreases pancreatic and liver tissue LTB4 levels. One week after induction of acute pancreatitis, LTC4 increases significantly in the liver and pancreas and this increase is inhibited by octreotide. LTs play an important role in the pathogenesis of cerulein-induced acute pancreatitis in rats.Öğe Platelet-activating factor and P-selectin activities in thrombotic and nonthrombotic Behçet's patients(2005) Tunc S.E.; Aksu K.; Keser G.; Oksel F.; Doganavsargil E.; Pirildar T.; Turk T.; Terzioglu E.; Huseyinov A.Objective: The aim of this study was to compare plasma Platelet-activating factor (PAF) and P-selectin (CD62P) activities in Behçet's disease patients with and without thrombosis. Methods: In this cross-sectional and descriptive study, 30 consecutive Behçet's patients were included, 15 of them with venous thrombosis. All patients were also divided into two subgroups according to the presence or absence of clinical activity. Plasma PAF levels, basal and Ca++ ionophore (A23187)-induced leukocyte (cellular) PAF activities, and platelet-rich plasma ?CD62P activity (the mean fluorescent density difference between CD62P phycoerythrin-positive and -negative stains) were evaluated. Results: In the thrombotic group, plasma PAF (P=0.001), basal leukocyte PAF (P=0.017), induced leukocyte PAF (P=0.024), and ?CD62P (P=0.023) levels were significantly higher than in the nonthrombotic group. In the whole group of Behçet's patients, there was a positive correlation between plasma PAF and ?CD62P levels (r=0.533, P=0.002). When we compared clinically active and inactive patients with respect to the above parameters, there was no significant difference, irrespective of thrombosis. Plasma PAF (P=0.001), basal leukocyte PAF (P=0.004), and ?CD62P (P=0.038) levels were significantly higher in the presence of both clinical activity and thrombosis than of clinical activity alone. Conclusion: Platelet-activating factor and CD62P may contribute to endothelial injury and thrombosis development in Behçet's disease. These two parameters seem related to the presence of thrombosis rather than clinical activity. © Springer-Verlag 2004.Öğe The Role of Dietary Supplementation with L-Glutamine in Inflammatory Mediator Release and Intestinal Injury in Hypoxia/Reoxygenation-Induced Experimental Necrotizing Enterocolitis(2003) Akisu M.; Baka M.; Huseyinov A.; Kultursay N.Background/Aims: Necrotizing enterocolitis (NEC) is a multifactorial syndrome in the neonate. Enteral feeding practices are an important component of gastrointestinal injury in neonatal NEC. In the present study, we examined the protective effect of oral supplementation with L-glutamine, an important specific fuel for the enterocytes, against hypoxia-reoxygenation (H/R)-induced NEC in young mice. Methods: Young mice were divided into four groups: group 1 mice (untreated) underwent H/R; group 2 mice were supplemented with L-glutamine in drinking water (0.5 g/dl) for 3 days, and group 3 mice were supplemented with L-glutamine (3 g/dl) for 10 days. Group 4 mice served as control. Hypoxia was induced by placing the young mice in a 100% CO2 chamber for 5 min. After hypoxia, they were reoxygenated for 10 min with 100% oxygen. We examined the intestinal lesions with light microscopy and measured intestinal generation of PAF and TNF-? in the H/R-induced model of NEC. Results: In group 3 mice, NEC-induced intestinal tissue damage was greatly attenuated with necrosis limited partially to the mucosa. Both intestinal tissue PAF and TNF-? concentrations were significantly higher in the untreated group than in controls (p < 0.001). Group 3 mice (3 g/dl supplemented) showed a significant decrease in intestinal TNF-? concentration compared with young group 1 and group 2 mice (p < 0.05 and p < 0.05, respectively). On the other hand, no significant difference was observed in the intestinal generation of PAF between H/R groups (p > 0.05). Conclusion: The present study suggests that H/R plays an important role in the pathogenesis of NEC and supports the hypothesis that especially PAF and TNF-? are involved in the pathophysiological mechanism of H/R-induced NEC. This study also demonstrates that dietary supplementation with L-glutamine reduces the histologic evidence of H/R-induced intestinal injury. Based on these findings, beneficial effects of L-glutamine in this model of NEC are mediated via mechanisms inhibiting intestinal cytokine release. Copyright © 2003 S. Karger AG, Basel.Öğe Supplementation with Saccharomyces boulardii Ameliorates Hypoxia/Reoxygenation-Induced Necrotizing Enterocolitis in Young Mice(2003) Akisu M.; Baka M.; Yalaz M.; Huseyinov A.; Kultursay N.Intestinal bacterial proliferation is an important aspect of gastrointestinal injury in neonatal necrotizing enterocolitis (NEC). In the present investigation, we examined the protective action of oral supplementation with Saccharomyces boulardii (S. boulardii), non-pathogen probiotic yeast, against hypoxia-reoxygenation (H/R)-induced NEC in young mice. Young mice were divided into three groups; Group 1 mice (untreated) were subjected only to hypoxia-reoxygenation; Group 2 mice were subjected to hypoxia-reoxygenation and were then given lyophilized S. boulardii (10 mg suspended in 0.5 ml saline) twice a day by orogastric intubation for 10 days. Group 3 mice served as controls. Hypoxia was induced by placing young mice in a 100% CO2 chamber for 5 min. After hypoxia, the young mice were reoxygenated for 10 min with 100% oxygen. We examined the intestinal lesions by light microscopy and measured intestinal generation of PAF and TNF-alpha in the H/R-induced model of NEC. In the probiotic group, NEC-induced intestinal tissue damage was greatly attenuated, with necrosis partially limited to the mucosa. Both intestinal tissue PAF and TNF-alpha concentrations were significantly higher in the untreated group than in controls (p < 0.001). S. boulardii-supplemented young mice showed a significant decrease in intestinal generation of PAF compared with untreated young mice (p < 0.05). On the other hand, no significant difference was observed in the intestinal concentration of TNF-alpha between untreated and probiotic groups (p > 0.05). The present study suggests that hypoxia/reoxygenation plays an important role in the pathogenesis of NEC and supports hypothesis that especially PAF and TNF-alpha are involved in the pathophysiological mechanism of H/R-induced NEC. This study also demonstrates that dietary supplementation with S. boulardii ameliorates the histologic evidence of H/R-induced intestinal injury. Based on these findings, the beneficial effects of probiotic S. boulardii in this model of NEC are mediated via mechanisms inhibiting intestinal proinflammatory mediator release.
