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

DNA polymerase α (calf):61 μM (IC50), DNA polymerase β (rat):108 μM (IC50)

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.