Gallic acid (GA, 3,4,5-trihidroxibenzoic) is a phenolic compound, widely represented in the plant kingdom, which has been demonstrated to exert beneficial health effects, including antihypertensive effect . The aim of this study was to evaluate the chronic antihypertensive effect of GA in hypertensive cafeteria diet-fed rats and the mechanisms involved in this effect. After 8 weeks of cafeteria diet feeding, male Wistar rats (n=6 per group) were daily orally supplemented with GA (6.65 mg/kg), Captopril (50 mg/kg) as a positive control or vehicle as a negative control for 3 weeks. Systolic blood pressure (SBP) and diastolic blood pressure (DBP) were measured by the tail cuff method and thoracic aorta was extracted to evaluate endothelium-dependent genes expression. After 3 weeks of GA administration, there was a significant reduction in blood pressure (BP) (-20 mmHg decrement of SBP and -15 mmHg decrement on DBP) when compared to animals from the vehicle group. Regarding gene expression, GA produced the upregulation of Sirt-1 and eNOS gene expression resulting in an increase of NO production and promoting a vasodilatation effect. In addition, GA downregulated the gene expression of the vasoconstrictor agent, ET-1, which could contribute to BP reduction observed after GA administration. Moreover, the antihypertensive effect of GA could be explained through the overexpression of NOX4 which has been reported to exert vasoprotective effects. Considering these results, we can conclude that GA had chronic antihypertensive effect in cafeteria diet-fed rats through an improvement in the endothelial function.
This work was supported by grant number AGL-2013-40707-R from the Spanish Government and grant number 2014LLAV00081 from Generalitat de Catalunya through Agència de Gestió d'Ajuts Universitaris i de Recerca (AGAUR) and the European Union through the European Regional Development Fund (FEDER).