In vitro and ex vivo antioxidant and vasodilatory properties of Syzygium cumini, Piper sarmentosum roxB and Psidium guajava plant extracts from Reunion Island

Abstract

Ischemic heart disease is the leading cause of cardiovascular death. It may originate from large vessel obstruction or from coronary microvascular dysfunction (CMD). CMD is associated with oxidative stress, which induces endothelial dysfunction and therefore alters vasodilation. The potentially beneficial cardiovascular effects of plant extracts have long been suggested by traditional medicine. We investigated the antioxidant and vasodilatory potential of 5 extracts from 3 plants from Reunion Island on in vitro and ex vivo experimental models. Aqueous extracts (AE) of Piper sarmentosum roxB (PSR) roots, PSR leaves, Psidium guajava (PG) leaves, a methanolic extract (ME) of Syzygium cumini (SC) seeds, and a hydroalcoholic extract (HE) of SC fruits were obtained. Their antioxidant capacities were assessed using DPPH (2,2DiPhenyle-1-Picryl-Hydrazyle). Concentrations of extracts ranged from 5 to 40 μg/mL in order to determine EC50 and T-EC50 values. To assess the vasodilatory potential of the extracts, phenylephrine-precontracted aortic rings from male Sprague Dawley rats with > 60% endothelium-dependent vasodilation were incubated with the extracts (50 μg/mL). Extracts displaying a vasodilatory effect were then used at 0.5, 5, and 50 μg/mL on precontracted aortic rings with (> 60%) or without (< 10%) endothelium. Finally, the pathway involved in endothelium-dependent relaxation by the extract was investigated by preincubation with the nitric oxide synthase (NOS) inhibitor L-NAME. The results are presenting in Table 1 . A high antioxidant capacity was observed for SC seed ME (EC50 = 8.0 μg/mL; T-EC50 = 10 min) and PG AE (EC50 = 9.7 μg/mL; T-EC50 = 15 min). SC seed ME and PG AE also demonstrated a vasodilatory effect (respectively: 64 ± 12% and 55 ± 17% vs. 4 ± 9% for control, P < 0.0001). No vasodilation was observed following endothelium removal. L-NAME significantly inhibited the vasodilatory effect of SC seed ME (32 ± 19% vs. 67 ± 15%, P = 0.003), but not that of PG (38 ± 19% vs. 66 ± 30%, P = 0.7). SC seed and PG demonstrated promising potential to prevent CMD due to their antioxidant properties and endothelium-dependent vasodilatory effects, with the effect of SC seed effect involving endothelial NOS. Further studies are warranted to determine the in vivo potential of these extracts.