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1
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Indirect role of beta2-adrenergic receptors in the mechanism of anti-inflammatory action of NSAIDs

100%
Suleyman H., Halici Z., Cadirci E., Hacimuftuoglu A., Bilen H.
Journal of Physiology and Pharmacology
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2008
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tom 59
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nr 4
661-672
In this study we investigated both intact and adrenalectomized rats to determine whether or not the anti-inflammatory effects of indomethacin, diclofenac sodium, ibuprofen, nimesulide, tenoxicam and aspirin (IDINTA) are related to adrenal gland hormones in carrageenan-induced inflammation model of rats. Also, we investigated the anti-inflammatory action mechanism of hormones (adrenalin, cortisol) which perform a role in the anti-inflammatory effect of IDINTA on the adrenergic receptors. The results show that IDINTA produces significant anti-inflammatory effects in intact rats (ID50: 9.82, 10.81, 95.21, 75.23, 8.21 and 61.84 mg/kg), but insignificant effects in adrenalectomized rats (ID50: 152.97, 188.17, 1275.0, 433.67, 188.16 and 1028.17 mg/kg). In addition, adrenalin and prednisolone caused anti-inflammatory effect rates of 78.3% and 95.7% respectively in adrenalectomized rats. The anti-inflammatory effects of adrenalin and prednisolone did not change when prazosin (1-receptor blocker), yohimbine (2-receptor blocker) and phenoxybenzamine (1- and 2- receptor blocker) were given to rat groups; however, in adrenalectomized rats administered with propranolol (a non-selective blocker of ß1 and ß2-receptors) the anti-inflammatory effect of adrenalin was lost, and that of prednisolone decreased to 36.2%. It was also found that metoprolol (a selective blocker of ß1-receptors) did not alter the anti-inflammatory effects of the drugs. As a result, it was shown that anti-inflammatory effects of IDINTA are related to adrenalin and cortisol (corticosterone in rats). It was also determined for the first time that adrenalin (totally) and prednisolone (partially) triggered anti-inflammatory effects via the ß2-receptors but not via the 1, 2 and ß1-receptors.
2
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The role of prednisolone and epinephrine on gastric tissue and erythrocyte antioxidant status in adrenalectomized rats

100%
Yildirim A., Sahin Y. N., Suleyman H., Yilmaz A., Yildirim S.
Journal of Physiology and Pharmacology
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2007
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tom 58
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nr 1
It has been believed that overproduction of free radicals and/or deficiency of antioxidant systems, and stress hormones may play a role in etiopathogenesis of many diseases, including gastric ulcer. This study evaluated whether there was an effect of adrenalectomy on lipid peroxidation [malondialdehyde (MDA)] and antioxidant [superoxide dismutase (SOD), glutathione peroxidase (GPX) and glutathione (GSH) levels] systems in gastric tissue and erythrocyte in rats. As well, the impacts of administration of prednisolone and epinephrine on these systems in adrenalectomized rats were investigated. Thirty-three rats were randomly grouped as sham-operated (group I), adrenalectomized (group II), adrenalectomized + prednisolone (group III) and adrenalectomized + epinephrine (group IV). After experimental procedures, blood and gastric tissues samples were taken from each animal in all groups. Colorimetric assays were employed to determine gastric tissue and erythrocyte levels of MDA and GSH, and SOD and GPX activities. Adrenalectomy in group II rats caused a marked decrease of SOD and GPX activities and MDA levels, and an increase of GSH levels in gastric tissue and erythrocyte, when compared to sham-operated rats. However, especially epinephrine injection after adrenalectomy resulted in a significantly increase of measured antioxidant enzyme activities and GSH levels in both gastric tissue and erythrocyte. These results indicate that adrenalectomy appeared to alter the levels of antioxidants and lipid peroxidation product in gastric tissue and erythrocyte. Thus, the present study provides a physiological regulatory role of adrenal gland in the maintenance of oxidant/antioxidant balance in gastric tissue and erythrocyte.
3
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Relation of adrenergic receptors, which have roles in gastroprotective and anti-inflammatory effect of adrenal gland hormones, with cyclooxygenase enzyme levels in rats

86%
Suleyman H., Dursun H., Bilici M., Cadirci E., Halici Z., Gulaboglu M., Albayrak F.
Journal of Physiology and Pharmacology
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2009
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tom 60
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nr 4
129-134
Background and Aims: COX-2 enzyme inhibition is responsible for the anti-inflammatory effects of NSAIDs, COX-1 for their effects upon the gastrointestinal system (GIS), along with other side effects. We investigated the relationship between COX levels and those adrenergic receptors known to play a role in gastroprotection and anti-inflammatory activity. Method: The effects of adrenaline and prednisolone on gastric COX-1 and COX-2 levels in both intact and adrenalectomized rats treated with doxazosin, yohimbine, propranolol, and metoprolol were determined. Results: We found that adrenaline increases COX-1 levels in the gastric tissue of both intact and adrenalectomized rats by stimulating -2 receptors. Adrenaline decreases COX-2 levels by stimulating ß-2 adrenergic receptors. Prednisolone inhibits both COX-1 and COX-2 in the gastric tissue of intact rats. In adrenalectomized rats, prednisolone increases gastric COX-1 by stimulating -2 receptors, and decreases COX-2 levels by stimulating ß-2 receptors. Conclusion: Prednisolone cannot bind to a adrenergic receptors in the presence of adrenaline (intact rats) but, in its absence (adrenalectomy), binds to -2 receptors, and stimulates them more effectively than adrenaline, suggesting a direct relationship between -2 adrenergic receptors and COX-1 levels, whereas ß-2 receptors are directly related to COX-2 levels.
4
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The prevention of ischemia/reperfusion induced oxidative damage by venous blood in rabbit kidneys monitored with biochemical, histopathological and immunohistochemical analysis

86%
Cetin N., Suleyman H., Sener E., Demirci E., Gundogdu C., Akcay F.
Journal of Physiology and Pharmacology
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2014
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tom 65
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nr 3
5
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Prevention of ischemia-reperfusion injury in rat ovarian tissue with the on-off method

72%
Ingec M., Isaoglu U., Yilmaz M., Calik M., Polat B., Alp H. H., Kurt A., Gundogdu C., Suleyman H.
Journal of Physiology and Pharmacology
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2011
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tom 62
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nr 5
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