Person: YEGEN, BERRAK
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YEGEN
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BERRAK
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Publication Metadata only Bombesin ameliorates colonic damage in experimental colitis(1999) YEGEN, BERRAK; Güllüoğlu, B. M.; Kurtel, H.; Güllüoğlu, M. G.; Aktan, A. O.; Yeğen, B. C.; Dizdaroğlu, F.; Yalin, R.; Yeğen, B. C.In the present study we investigated the possible therapeutic effects of bombesin on an experimentally induced colitis model in rats. Inflammation of the colon was induced by a single intracolonic administration of 30 mg of 2,4,6-trinitrobenzene sulfonic acid (TNBS) at 8 cm from the anus. Immediately after the induction of colitis, some rats were given bombesin (10 microg/kg; subcutaneously) three times a day for 14 days, while another group received vehicle treatment. On day 14, the rats were decapitated and plasma carbonyl content and tissue myeloperoxidase level, as an index of granulocyte infiltration into intestinal tissue, were determined in order to obtain an objective evaluation of colonic injury. In the colitis group, increased macroscopic damage score, elevated MPO level and high plasma carbonyl content, together with the microscopic appearance revealed severe inflammatory changes resembling IBD. Bombesin treatment attenuated the TNBS-induced colonic damage and stimulated histopathologically apparent mucosal proliferation, suggesting that bombesin may play a role in protecting gut integrity.Publication Metadata only Pathways mediating CRF-induced inhibition of gastric emptying in rats(1997) YEGEN, BERRAK; Coşkun, T.; Bozkurt, A.; Alican, I.; Ozkutlu, U.; Kurtel, H.; Yegen, B. C.The corticotrophin-releasing factor (CRF) is shown to be released during stress suggesting that CRF has a physiological role in the mediation of central nervous system (CNS) response to stress, including an inhibitory effect on gastric emptying. In the present study, we have examined the pathways by which intracerebroventricularly (i.c.v.) administered CRF and central CRF activation during stress alter the gastric emptying rate of saline (0.14 M), acid (50 mM), peptone (4.5%) and peptone after preload. The emptying rates of all these test meals were significantly (p < 0.05-0.001) delayed with increasing doses of i.c.v. CRF (0.001, 0.003, 0.01, 0.1, 0.3 and 1 nmol/10 microl), when compared with their i.c.v. saline-treated controls. The 1-nmol dose of CRF inhibited the emptying of acid, peptone and peptone after a preload by 43.8%, 64.1% and 81.1%, respectively. Twenty-minute swim stress delayed gastric emptying rate of saline, acid and peptone solutions significantly (p < 0.001) and the CRF receptor antagonist, alpha-helical CRF (8 nmol/10 microl, i.c.v.), applied before the swim stress, abolished the inhibitory effect of stress on the emptying rate of these solutions. Acute intragastric administration of capsaicin (2 mg/rat) and systemic capsaicin (125 mg kg(-1)) treatment facilitated the gastric emptying rate of acid, peptone and peptone after preload significantly, almost abolishing the inhibitory effect of central CRF (p < 0.001). However, either capsaicin treatment had no effect on stress-induced inhibition of the gastric emptying of none of the solutions, except peptone after a preload. Our findings demonstrate that the gastric inhibitory response induced by swimming as a stress-producing stimulus is mediated by the endogenous release of CRF. They also suggest that CRF exerts its CNS actions on the gastrointestinal tract via vago-vagal, capsaicin-sensitive pathways, probably involving the central cholecystokinin (CCK) mechanisms.Publication Metadata only Effect of cold-restraint stress on glutathione and lipid peroxide levels in the liver and glandular stomach of rats(1990) YALÇIN, AHMET SUHA; Yeğen, B.; Dedeoğlu, A.; Aykaç, I.; Oktay, S.; Yalçin, A. S.The effect of starvation and cold-restraint stress on glutathione and lipid peroxide levels in the liver, stomach and plasma of rats was investigated. Hepatic and gastric glutathione levels were significantly decreased in starvation and cold-restraint groups when compared with values obtained from the control group. In both tissues, lipid peroxide levels were significantly decreased after starvation but were not significantly different from control values after cold-restraint treatment. However, when compared with the values obtained from the starvation group there was a significant increase in both hepatic and gastric lipid peroxide levels after cold-restraint. Plasma lipid peroxide levels were slightly decreased in the starvation group and significantly increased in the cold-restraint group. Our results suggest that pathological consequences of stress on different tissues could be due to stimulation of lipid peroxidation.Publication Metadata only Inflammatory response to cold injury in remote organs is reduced by corticotropin-releasing factor(2001) YEGEN, BERRAK; Bozkurt, A.; Ghandour, S.; Okboy, N.; Oner, S.; Arbak, S.; Coşkun, T.; Yeğen, B. C.Current experimental evidence concerning the potential activity of corticotropin releasing factor (CRF) in inflammatory processes still remains controversial. To determine whether CRF has protective effects on three remote organs (liver, lung and stomach) affected by cold injury and to characterize the role of neutrophils in cold-induced inflammation, dorsums of anesthetized rats were exposed for 5 min to a 22% NaCl solution maintained at -20+/-0.5 degrees C and the rats were sacrificed at 24 h after the cold injury. The results indicate that cold-exposure-induced edema in the liver, lung and stomach was blocked by subcutaneous (s.c.; 1.2 and 12 nmol/kg; 30 min before cold trauma) CRF pretreatment, while the central administration of CRF (intracisternally (i.c.); 0.30 and 1.5 nmol/rat; 15 min before cold) had the similar effect at the higher dose. Histological assessment and the tissue myeloperoxidase activities also revealed that CRF given peripherally has a protective role in damage generation. Moreover, CRF had a facilitatory effect in the recovery of the body temperature following cold exposure. In conclusion, CRF is likely to act on its peripheral receptors in the inflamed remote organs, suppressing the edematogenic effects of inflammatory mediators, some of which are neutrophil-derived.Publication Metadata only Melatonin ameliorates oxidative organ damage induced by acute intra-abdominal compartment syndrome in rats(2003) YEGEN, BERRAK; Sener, Göksel; Kaçmaz, Ayhan; User, Yilmaz; Ozkan, Sirri; Tilki, Metin; Yeğen, Berrak C.Acutely increased intra-abdominal pressure (IAP) can lead to multiple organ failure. As blood flow to intra-abdominal organs is reduced by high venous resistance, ischemia-reperfusion (I/R) injury plays an important role in the pathogenesis of abdominal compartment syndrome (ACS) following IAP. Melatonin, a secretory product of the pineal gland, is known to have free radical scavenging and antioxidative properties in several oxidative processes. The objective of this study was to examine the potential protective properties of melatonin on the oxidative organ damage in a rat model of ACS. Under ketamine anesthesia, an arterial catheter was inserted intraperioneally (i.p.) and using an aneroid manometer connected to the catheter, IAP was kept at 20 mmHg (ischemia group; I) for 1 hr. In the ischemia/reperfusion (I/R) group, pressure applied for an hour was decompressed and a 1-hr reperfusion period was allowed. In another IR group, melatonin was administered (10 mg/kg, i.p.) immediately before the decompression of IAP. The results demonstrate that tissue levels of malondialdehyde (MDA) and myeloperoxidase activity (MPO; index of tissue neutrophil infiltration) were elevated, while glutathione (GSH; a key to antioxidant) levels were reduced in both I and I/R groups (P < 0.05-0.001). Melatonin treatment in I/R rats reversed these changes (P < 0.01-0.001). Moreover, melatonin given to the I/R group reduced the elevations in serum aspartate aminotransferase, alanine aminotransferase and blood urea nitrogen levels and abolished the increase in serum creatinine levels. Our results indicate that melatonin, because of antioxidant and free radical scavenging properties, ameliorates reperfusion-induced oxidative organ damage. In conclusion, the results of the present study suggest that the therapeutic value of melatonin as a 'reperfusion injury-limiting' agent must be considered in ACS.Publication Metadata only Oxidative organ damage in a rat model of thermal injury: the effect of cyclosporin A(1997) YEGEN, BERRAK; Gürbüz, V.; Corak, A.; Yeğen, B. C.; Kurtel, H.; Alican, I.Animal models of thermal trauma implicate oxygen radicals as a causative agent in local wound response, development of burn shock and distant organ injury. It has been proposed that the source of reactive oxygen metabolites could be neutrophils sequestered in systemic organs as a result of the systemic inflammatory reaction to a local burn insult. Recent studies have suggested that cyclosporin A (CsA), a potent immunosuppressive drug, may have effects on neutrophils by modulating the rate of their accumulation during acute inflammatory reactions. This study aimed to assess the role of neutrophils in the early and late phases of burn injury in rats with second-degree skin burn. We also aimed to determine whether CsA has protective effects on organs remote from the thermal injury. The results demonstrate that there is significant neutrophil accumulation in the gastric mucosa, liver and lung tissues during the early phase of a burn injury and that CsA failed to protect these organs. In conclusion, the data of this study suggest that neutrophil accumulation in liver, lung and gastric mucosa following burn injury may be involved in the pathogenesis of remote organ damage. The results also indicate that CsA failed to reduce the severity of damage in these organs, probably due to its own toxic effects.Publication Metadata only The alterations of leukotriene C4 and prostaglandin E2 levels following different ischemic periods in rat brain tissue(1991) YEGEN, BERRAK; Aktan, S.; Aykut, C.; Oktay, S.; Yegen, B.; Keles, E.; Aykaç, I.; Ercan, S.Leukotrienes and prostaglandins are formed from arachidonic acid by activation of local phospholipases in pathological conditions such as cerebral ischemia, subarachnoid hemorrhage, cerebral tumors and seizures. These mediators, especially leukotrienes have a very potent vasoconstrictor effect on cerebral arteries. Experimental studies have shown that this effect, by increasing vascular permeability causes vasogenic edema that contributes to the ischemic penumbra. In this study, after developing an experimental animal model simulating the concept of ischemic penumbra in the rat, the levels of leukotriene C and prostaglandin E2 produced in the forebrain were measured and the effects of these mediators in prolonged ischemia were investigated. The results, in the first 4 min of ischemia, showed that the arachidonic acid metabolites, particularly, leukotriene C4, reached a peak in the ischemic cerebral tissue in association with leukocyte accumulation. Later in the 15th min, significant decreases in leukotriene C4 and prostaglandin E2 levels were seen. In the 1st and 4th h, probably due to the stimulation of the relevant enzymes by free oxygen radicals in the ischemic tissue; the levels increase again, returning to control values by the 12th h. It is concluded that the use of lipoxygenase inhibitors and free radical scavengers may be helpful to limit the infarct area in the first 4 h of ischemia.Publication Metadata only The effect of nordihydroguaiaretic acid on leukotriene C4 and prostaglandin E2 production following different reperfusion periods in rat brain after forebrain ischemia correlated with morphological changes(1993) YEGEN, BERRAK; Aktan, S.; Aykut, C.; Yegen, B. C.; Okar, I.; Ozkutlu, U.; Ercan, S.Leukotriene C4 (LTC4) and prostaglandin E2 (PGE2) are the 5-lipoxygenase and cyclooxygenase metabolites of arachidonic acid (AA). They constrict blood vessels and enhance vascular permeability inducing vasogenic edema that may hurt the ischemic penumbra after cerebral ischemia and reperfusion. Nordihydroguaiaretic acid (NDGA) is known as the most potent inhibitor of 5-lipoxygenase in different tissues. Furthermore, it has considerable inhibitory activity against cyclooxygenase. In this study, after developing a global ischemic model in the rat, the levels of LTC4 and PGE2 in the forebrain were measured, following different reperfusion periods after 10 min ischemia including 8 rats for each reperfused group. Sham operations were performed for each corresponding control group (n = 8). AA metabolites were then correlated with neuropathological findings. In the combined reperfused groups both metabolites increased significantly when compared with 10 min, ischemic group (P < 0.05). In the 8 min reperfused group, PGE2 and LTC4 increased significantly compared with each corresponding control group (P < 0.005). These mediators also increased to high levels compared with the 4 min reperfused group (P < 0.05, P < 0.005). PGE2 and LTC4 were reduced significantly at the 15th and 60th min of reperfusion compared with the 8 min reperfused group (P < 0.05, P < 0.005). NDGA (0.1 mg/kg) reduced both metabolites in the 8 min reperfused group significantly (P < 0.05). Brain cortex specimens were taken for light and electromicroscopical investigations. No significant differences were noted between the structural changes in the 4, 8 and 15 min of reperfusion and NDGA administered groups.(ABSTRACT TRUNCATED AT 250 WORDS)Publication Metadata only Bombesin improves burn-induced intestinal injury in the rat(2000) YEGEN, BERRAK; Alican, I.; Unlüer, E. E.; Yeğen, C.; Yeğen, B. C.This study was designed to determine the effect of exogenous bombesin (10 microg/kg/day, subcutaneously, three times a day) on intestinal hypomotility and neutrophil infiltration in the early and late phases of burn injury (partial-thickness, second-degree burn of the skin). In acute (2 h after burn injury) or chronic (3 days after) burn groups, intestinal transit was delayed, which was reversed by bombesin treatment. In the acute burn group, but not in the chronic group, increased MPO activity was also reduced by bombesin treatment. The results demonstrate that bombesin ameliorates the intestinal inflammation due to burn injury, involving a neutrophil-dependent mechanism.Publication Metadata only The effect of aqueous garlic extract on the levels of arachidonic acid metabolites (leukotriene C4 and prostaglandin E2) in rat forebrain after ischemia-reperfusion injury(1996) YEGEN, BERRAK; Batirel, H. F.; Aktan, S.; Aykut, C.; Yeğen, B. C.; Coşkun, T.Leukotriene C4 (LTC4) and prostaglandin E2 (PGE2) are known to be highly potent cerebral vasoconstrictors which are formed from arachidonic acid (AA). They enhance vascular permeability, inducing vasogenic edema that may damage the ischemic penumbra after ischemia and reperfusion. The inhibitory effect of aqueous garlic extract (AGE) on AA metabolism in human platelets is known. In this study, following the global ischemic model application to the rats, all underwent 10 min ischemia and were reperfused for different periods. The levels of LTC4 and PGE2 in rat forebrain were then measured. One rat group consisted of 8 rats. In the combined reperfused groups both metabolites increased significantly when compared with the 10 min ischemia alone, no reperfusion group (p < 0.05). In the 8 min reperfused group, PGE2 and LTC4 levels increased significantly at 60 min of reperfusion compared with each corresponding control group (P < 0.005). PGE2 and LTC4 levels were reduced significantly at 60 min of reperfusion compared with the 8 min reperfused group (P < 0.005). AGE (1 ml/kg) reduced both LTC4 and PGE2 levels significantly in the 8 min and 60 min reperfused group (P < 0.001, P < 0.001, P < 0.05, P < 0.01). In conclusion, AGE reduced LTC4 and PGE2 levels at a dosage of 1 ml/kg following 8 and 60 min reperfusion. It may be helpful in reducing AA metabolite levels and preventing injury after ischemic phenomena.
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