{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T13:56:21Z","timestamp":1787320581779,"version":"build-2736575974"},"reference-count":42,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2021,8,9]],"date-time":"2021-08-09T00:00:00Z","timestamp":1628467200000},"content-version":"vor","delay-in-days":220,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001700","name":"Ministry of Education, Culture, Sports, Science and Technology","doi-asserted-by":"publisher","award":["19K09086"],"award-info":[{"award-number":["19K09086"]}],"id":[{"id":"10.13039\/501100001700","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Oxidative Medicine and Cellular Longevity"],"published-print":{"date-parts":[[2021,1]]},"abstract":"<jats:p>\n                    Despite remarkable scientific advances in the understanding of molecular mechanisms for sepsis, therapeutic options are far from satisfactory. High mobility group box 1 (HMGB1), one of the ligands of receptor for advanced glycation end products (RAGE), is a late mediator of lethality in septic mice. We have recently found that the DNA\u2010aptamer raised against RAGE (RAGE\u2010aptamer) significantly blocks experimental diabetic nephropathy and melanoma growth and metastasis. We examined the effects of RAGE\u2010aptamer on sepsis score, survival rate, and inflammatory and oxidative stress responses in serum, peripheral monocytes, kidneys and livers of lipopolysaccharide\u2010 (LPS\u2010) injected mice, and on LPS\u2010exposed THP\u20101 cells. RAGE\u2010aptamer inhibited the binding of HMGB1 to RAGE\n                    <jats:italic>in vitro<\/jats:italic>\n                    . RAGE\u2010aptamer significantly (\n                    <jats:italic>P<\/jats:italic>\n                    = 0.002) improved sepsis score at 8 hours after LPS injection and survival rate at 24 hours (\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.01, 70%) in septic mice compared with LPS+vehicle\u2010 or LPS+control\u2010aptamer\u2010treated mice. RAGE\u2010aptamer treatment significantly decreased expression of p\u2010NF\u2010\n                    <jats:italic>\u03ba<\/jats:italic>\n                    B p65, an active form of redox\u2010sensitive transcriptional factor, NF\u2010\n                    <jats:italic>\u03ba<\/jats:italic>\n                    B and gene or protein expression of TNF\u2010\n                    <jats:italic>\u03b1<\/jats:italic>\n                    , IL\u20101\n                    <jats:italic>\u03b2<\/jats:italic>\n                    , IL\u20106, and HMGB1 in serum, peripheral monocytes, and kidneys of septic mice in association with the reduction of oxidative stress and improvement of metabolic acidosis, renal and liver damage. LPS\u2010induced oxidative stress, inflammatory reactions, and growth suppression in THP\u20101 cells were significantly blocked by RAGE\u2010aptamer. Our present study suggests that RAGE\u2010aptamer could attenuate multiple organ damage in LPS\u2010injected septic mice partly by inhibiting the inflammatory reactions via suppression of HMGB1\u2010RAGE interaction.\n                  <\/jats:p>","DOI":"10.1155\/2021\/9932311","type":"journal-article","created":{"date-parts":[[2021,8,9]],"date-time":"2021-08-09T20:35:05Z","timestamp":1628541305000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["DNA\u2010Aptamer Raised against Receptor for Advanced Glycation End Products Improves Survival Rate in Septic 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