Euscaphic acid has anti-diabetic, and anti-inflammatory activities, it inhibits LPS-induced inflammatory responses by interference with the clustering of TRAF6 with IRAK1 and TAK1, resulting in blocking the activation of IKK and MAPKs signal transduction

Isolated aorta was used to test the anti-contraction effects and the possible mode of action(s) of the EA (1*10 -7 M) and (3*10 -7 M) isolated from Crataegus azarolus var. aronia L. Euscaphic acid showed high anti-contraction effects on norepinephrin (NE), (1*10 -9 -10 -4 M) induced contraction in aortic smooth muscle cells in endothelium-intact, endothelium-denuded, and aortic rings pre-incubated with potassium (K + )-channels blocker (tetraethylammonium, TEA), prostaglandin I 2 (PGI ) inhibitor (indomethacin) and cyclic guanosine monophosphate (cGMP) inhibitor ( methylene blue). On the other hand, other K 2 channels subtype blockers glibenclamide (GLIB); barium chloride (BaCl ) and 4-aminopyridine (4-AP) demonstrated that adenosine triphosphate sensitive K + (K ATP ), inwardly rectifying K 2 + (K ir ) and voltage-dependent K ) channels played no role in anti-contraction induced by EA. Furthermore, the role of L-types calcium (Ca ) channels in EA anti-contractile effects on aortic smooth muscle cells was proved, by using the Ca -channel blocker verapamil, as indicated by the production of a potent anti-contraction effect . The results of the current study indicate that the anti-contraction effects of EA may be due to the activation of calcium dependent, K ) channels and blocking of L-type Ca ++ channels.