Sulfur dioxide improves endothelial dysfunction by downregulating the angiotensin II/AT1R 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 (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.