Quercetin and catechin synergistically inhibit angiotensin II-induced redox-dependent signalling pathways in vascular smooth muscle cells from hypertensive rats

Abstract

Dietary flavonoids, present in different amount in foods, are associated with the prevention of hypertension, but little is known about the interactions between them. The aim of this study was to explore the effect of quercetin (Q), catechin (C) and the mixture, on Angiotensin II (AngII)-induced redox-dependent signalling pathways and cell behaviour. Mesenteric smooth muscle cells (MesSMC) from spontaneously hypertensive rats (SHR) were incubated with AngII (0.1 μmol/L) alone, or with the mixture of low concentrations of Q and C. AngII-increased ROS production was reduced by the mixture of separately ineffective low concentration of Q (15 μmol/L) plus C (20 μmol/L). This mixture reduced AngII-stimulated NAD(P)H oxidase activation and p47phox translocation to the cell membrane, without affecting Nox2 expression. Co-incubation of Q + C significantly inhibited AngII-induced migration and proliferation, and these effects were independent of p-ERK1/2 and related with reduced p38MAPK phosphorylation. These findings demonstrated that low concentrations of singly non-effective flavonoids when are combined exert a synergistic effect in inhibiting AngII-induced redox-sensitive signalling pathways.

Catechin and quercetin attenuate adipose inflammation in fructose‐fed rats and 3T3‐L1 adipocytes

“…Some in vitro studies have shown a synergistic effect of C and Q on the inhibition of collagen‐induced platelet aggregation and platelet adhesion . C and Q also synergistically inhibit angiotensin II induced redox‐dependent signaling pathways in vascular smooth muscle cells from hypertensive rats , while no synergistic effects were observed in pulmonary vascular smooth muscle . Other study that evaluated the antiproliferative effects of Q, C, and epicatechin in three different cancer cell lines showed that only Q possesses antiproliferative activity , suggesting that these compounds may have different mechanisms of action.…”

Ethyl Acetate Fraction and Isolated Phenolics Derivatives from Mandevilla moricandiana Identified by UHPLC-DAD-ESI-MSn with Pharmacological Potential for the Improvement of Obesity-Induced Endothelial Dysfunction

“…The phytochemical analysis of MMEAF revealed the presence of different phenolic compounds that have protective vascular effects, which could additively and/or synergistically contribute to the effects of this fraction on aorta from obese rats. Studies have shown that polyphenolic mixtures present synergistic and additive antioxidant and vascular effects [ 76 , 77 , 78 , 79 ]. In this respect, quercetin and kaempferol synergistically acted in the reduction in H 2 O 2 -induced oxidative stress [ 80 ].…”

Quercetin Attenuates Ethanol‐Induced Iron Uptake and Myocardial Injury by Regulating the Angiotensin II‐L‐Type Calcium Channel

“…Moreover, some studies have shown that quercetin antagonizes Ang II‐induced apoptosis of human umbilical vein endothelial cells as well as myocardial hypertrophy . In addition, quercetin has also been reported to regulate the proliferative and migratory response of VSMCs during Ang II‐induced hypertension …”