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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.
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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
|
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.
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