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. 2017 Jul 7;114(30):E6034–E6043. doi: 10.1073/pnas.1610325114

Fig. 5.

Fig. 5.

Biological effects of 17,18-EEQ-EA and 19,20-EDP-EA on platelet aggregation, vasculature tension, and angiogenesis. The physiological functions of 17,18-EEQ-EA and 19.20-EDP-EA regioisomers were examined to characterize their effects on platelet aggregation, vasodilation, and angiogenesis. (A and B) In whole human blood, 17,18-EEQ-EA dose-dependently inhibited AA-induced platelet aggregation (n = 4) (A), whereas 19,20-EDP-EA induced platelet aggregation (B) under stirring conditions in the absence of a platelet agonist (n = 7). (C and D) Dose-dependent relaxation of bovine coronary arteries preconstricted with U-46619 (40 nM) was measured for 17,18-EEQ-EA and 17,18-EEQ (C) and for 19,20-EDP and 19,20-EDP-EA (D) to calculate the ED50. (E) 17,18-EEQ-EA and 19,20-EDP-EA were assessed for their ability to inhibit VEGF-promoted angiogenesis in HMVECs plated on Matrigel (n =7). Compounds were studied in parallel with each of their epoxide and ethanolamide parent compounds. All values are means ± SE; *P < 0.05, **P < 0.01, and ***P < 0.001.