Sulfur dioxide improves endothelial dysfunction by downregulating the angiotensin II/AT 1 R pathway in D-galactose-induced aging rats

摘要

The aim of this study was to investigate the protective effects of sulfur dioxide (SO₂) on the endothelial function of the aorta in D-galactose (D-gal)-induced aging rats. Sprague Dawley rats were randomized into a D-gal group, a D-gal + SO₂ group and a control group, then injected with D-gal, D-gal + SO₂ donor or equivalent volumes of saline, respectively, for 8 consecutive weeks. After 8 weeks, the mean arterial pressure was significantly increased in the D-gal group, but was lowered by SO₂. SO₂ significantly ameliorated the endothelial dysfunction induced by D-gal treatment. The vasorelaxant effect of SO₂ was associated with the elevated nitric oxide levels and upregulated phosphorylation of endothelial nitric oxide synthase. In the D-gal group, the concentration of angiotensin II in the plasma was significantly increased, but was decreased by SO₂. Moreover, levels of vascular tissue hydrogen peroxide (H₂O₂) and malondialdehyde were significantly lower in SO₂-treated groups than those in the D-gal group. Western blot analysis showed that the expressions of oxidative stress-related proteins (the angiotensin II type 1 receptor (AT₁R), and nicotinamide adenine dinucleotide phosphate oxidase subunits) were increased in the D-gal group, while they were decreased after treatment with SO₂. In conclusion, SO₂ attenuated endothelial dysfunction in association with the inhibition of oxidative stress injury and the downregulation of the angiotensin II/AT₁R pathway in D-gal-induced aging rats.