Abstract

The aim of this study was evaluated the anti‐inflammatory effects in vivo model of renovascular hypertension (RH) and in endothelial cells (ECs). Rats were treated with ASE 200 mg.kg‐1.day (or vehicle) for 40 days. Oxidative damage, antioxidant activity and the expression of endothelial nitric oxide synthase (eNOS), superoxide dismutase 1 and 2 (SOD 1 and 2), metalloproteinase (MMP‐2) and tissue inhibitor of metalloproteinases (TIMP)‐1 were determined. Structural changes in the aortic and mesenteric MMP‐2 levels were evaluated. In in vitro experiments, ECs were treated with 100 ug/mL of ASE and the expressions of inflammatory markers were evaluated. ASE reduced the increased mesentery levels of malondialdehyde and carbonyl protein in hypertensive rats. SOD, catalase and glutathione peroxidase activities and SOD1 and 2, eNOS and TIMP‐1 expressions were reduced. ASE prevented the vascular remodeling, as well as, the increased MMP‐2 expression and levels found in hypertensive rats. In ECs ASE was able to decreased TNFα, eNOS and IL‐8 mRNA expression. These results suggest that ASE prevents the endothelial dysfunction and vascular structural changes associated with hypertensionGrant Funding Source: FAPERJ, CNPq and CAPES

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