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

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 (H2 O2 ) 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 (AT1 R), 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/AT1 R pathway in D-gal-induced aging rats.