Thymoquinone-induced relaxation of isolated rat pulmonary artery

Aim of the studyThe effect of thymoquinone (TQ), the main constituent of the volatile oil of black seed (Nigella sativa L. family Ranunculaceae), on the isolated rat pulmonary arterial rings was investigated.Materials and methodsIsolated rat pulmonary arterial rings were precontracted with phenylephrine and concentration–response curves to TQ were constructed. The effects of different receptors antagonists or enzyme inhibitors were examined.ResultsTQ caused a concentration-dependent decrease in the tension of the pulmonary arterial rings precontracted by phenylephrine. The effects of TQ were not influenced by pretreatment of the rings with propranolol (a non-selective β-blocker), atropine (a non-selective blocker for muscarinic receptors), theophylline (an adenosine receptor antagonist), indomethacin (a cyclooxygenase inhibitor), L-NAME (a NO synthase inhibitor), methylene blue (an inhibitor of soluble guanylyl cyclase) and nifedipine (a Ca2+ channel blocker). The effects of TQ were significantly potentiated by bosentan (an ETA/ETB receptor antagonist). The effects of TQ were slightly abolished by pretreatment of the rings with glibenclamide (a non-selective blocker of ATP-sensitive K+ channels). TQ totally abolished the pressor effects of serotonin and phenylephrine on the isolated rat pulmonary arterial rings.ConclusionThe results of the present study suggest that TQ-induced relaxation of the precontracted pulmonary artery is probably mediated, at least in part, by activation of ATP-sensitive potassium channels and possibly by non-competitive blocking of serotonin, α1 and endothelin receptors.

The effect of thymoquinone (TQ) on the isolated rat pulmonary arterial rings was investigated. TQ caused a concentration-dependent decrease in the tension of the pulmonary arterial rings precontracted by phenylephrine. The results of the present study suggest that TQ-induced relaxation of the precontracted pulmonary artery is probably mediated, at least in part, by activation of ATP-sensitive potassium channels and possibly by non-competitive blocking of serotonin, α1 and endothelin receptors.Figure optionsDownload as PowerPoint slide