{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T01:58:01Z","timestamp":1777859881157,"version":"3.51.4"},"reference-count":54,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2018,5,31]],"date-time":"2018-05-31T00:00:00Z","timestamp":1527724800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Renin Angiotensin Aldosterone Syst"],"published-print":{"date-parts":[[2018,6,1]]},"abstract":"<jats:p>\n                    The aim of this study was to investigate the protective effects of sulfur dioxide (SO\n                    <jats:sub>2<\/jats:sub>\n                    ) 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 + SO\n                    <jats:sub>2<\/jats:sub>\n                    group and a control group, then injected with D-gal, D-gal + SO\n                    <jats:sub>2<\/jats:sub>\n                    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 SO\n                    <jats:sub>2<\/jats:sub>\n                    . SO\n                    <jats:sub>2<\/jats:sub>\n                    significantly ameliorated the endothelial dysfunction induced by D-gal treatment. The vasorelaxant effect of SO\n                    <jats:sub>2<\/jats:sub>\n                    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 SO\n                    <jats:sub>2<\/jats:sub>\n                    . Moreover, levels of vascular tissue hydrogen peroxide (H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    ) and malondialdehyde were significantly lower in SO\n                    <jats:sub>2<\/jats:sub>\n                    -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 (AT\n                    <jats:sub>1<\/jats:sub>\n                    R), and nicotinamide adenine dinucleotide phosphate oxidase subunits) were increased in the D-gal group, while they were decreased after treatment with SO\n                    <jats:sub>2<\/jats:sub>\n                    . In conclusion, SO\n                    <jats:sub>2<\/jats:sub>\n                    attenuated endothelial dysfunction in association with the inhibition of oxidative stress injury and the downregulation of the angiotensin II\/AT\n                    <jats:sub>1<\/jats:sub>\n                    R pathway in D-gal-induced aging rats.\n                  <\/jats:p>","DOI":"10.1177\/1470320318778898","type":"journal-article","created":{"date-parts":[[2018,5,31]],"date-time":"2018-05-31T08:04:54Z","timestamp":1527753894000},"update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":11,"title":["Sulfur dioxide improves endothelial dysfunction by downregulating the angiotensin II\/AT\n                    <sub>1<\/sub>\n                    R pathway in D-galactose-induced aging rats"],"prefix":"10.1177","volume":"19","author":[{"given":"Jing","family":"Dai","sequence":"first","affiliation":[{"name":"Department of Clinical Diagnostics, 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