{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T23:31:09Z","timestamp":1782948669060,"version":"3.54.5"},"reference-count":58,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2023,7,12]],"date-time":"2023-07-12T00:00:00Z","timestamp":1689120000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Environmental Toxicology"],"published-print":{"date-parts":[[2023,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Septic acute kidney injury (SAKI) is usually caused by sepsis. It has been shown that catalpol (Cat) impairs sepsis\u2010evoked organ dysfunction to a certain degree. The current work aims to evaluate the protective effects of Cat on SAKI and potential mechanisms in vivo and in vitro.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>SAKI cellular and murine model were set up using lipopolysaccharide (LPS) in vitro and in vivo. Cell apoptosis in cells was determined by TUNEL assay. Levels of inflammatory cytokines were detected by enzyme\u2010linked immunosorbent assay (ELISA). The levels of the markers of oxidative injury were evaluated by corresponding commercial kits. Protein levels were assayed via western blotting and immunohistochemistry (IHC) staining.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The results demonstrated that LPS upregulated TNF\u2010\u03b1, IL\u20106, and malondialdehyde levels, and downregulated superoxide dismutase, whereas Cat treated cells have the opposite results. Functional assays displayed that Cat remarkably reversed the LPS\u2010challenged damage as the impairment of TNF\u2010\u03b1 and IL\u20106 levels, oxidative stress, and the apoptosis in HK\u20102 cells. Moreover, knockdown of Sirtuin 1 (Sirt1) counteracted the suppressive impact of Cat on LPS\u2010triggered inflammatory response, oxidative stress, and renal damage. Further, Cat elevated Sirt1 expression and activated the Nrf2\/HO\u20101 signaling in LPS\u2010engendered SAKI in vivo and in vitro.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Our study clearly proved that Cat protected against LPS\u2010induced SAKI via synergic antioxidant and anti\u2010inflammatory actions by regulating Sirt1 and Nrf2\/HO\u20101 signaling pathways.<\/jats:p><\/jats:sec>","DOI":"10.1002\/tox.23855","type":"journal-article","created":{"date-parts":[[2023,7,12]],"date-time":"2023-07-12T14:30:27Z","timestamp":1689172227000},"page":"2182-2191","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Catalpol ameliorates inflammation and oxidative stress via regulating Sirt1 and activating Nrf2\/HO\u20101 signaling against acute kidney injury"],"prefix":"10.1002","volume":"38","author":[{"given":"Manli","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of 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