{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,6]],"date-time":"2026-11-06T11:28:15Z","timestamp":1793964495869,"version":"4.8.0"},"reference-count":41,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2022,12,31]],"date-time":"2022-12-31T00:00:00Z","timestamp":1672444800000},"content-version":"vor","delay-in-days":364,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100003453","name":"Natural Science Foundation of Guangdong Province","doi-asserted-by":"publisher","award":["2019A1515011817"],"award-info":[{"award-number":["2019A1515011817"]}],"id":[{"id":"10.13039\/501100003453","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81900347"],"award-info":[{"award-number":["81900347"]}],"id":[{"id":"10.13039\/501100001809","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":[[2022,1]]},"abstract":"<jats:p><jats:italic>Background<\/jats:italic>. Diabetes mellitus (DM) can induce cardiomyocyte injury and lead to diabetic cardiomyopathy (DCM) which presently has no specific treatments and consequently increase risk of mortality. <jats:italic>Objective<\/jats:italic>. To characterize the therapeutic effect of 6\u2010gingerol (6\u2010G) on DCM and identify its potential mechanism. <jats:italic>Methods<\/jats:italic>. In vivo streptozotocin\u2010 (STZ\u2010) induced DM model was established by using a high\u2010fat diet and STZ, followed by low\u2010dose (25\u2009mg\/kg) and high\u2010dose (75\u2009mg\/kg) 6\u2010G intervention. For an in vitro DCM model, H9c2 rat cardiomyoblast cells were stimulated with high glucose (glucose = 33\u2009mM) and palmitic acid (100\u2009<jats:italic>\u03bc<\/jats:italic>M) and then treated with 6\u2010G (100\u2009<jats:italic>\u03bc<\/jats:italic>M). Histological and echocardiographic analyses were used to assess the effect of 6\u2010G on cardiac structure and function in DCM. Western blotting, ELISA, and real\u2010time qPCR were used to assess the expression of ferroptosis, inflammation, and the Nrf2\/HO\u20101 pathway\u2010related proteins and RNAs. Protein expression of collagen I and collagen III was assessed by immunohistochemistry, and kits were used to assay SOD, MDA, and iron levels. <jats:italic>Results<\/jats:italic>. The results showed that 6\u2010G decreased cardiac injury in both mouse and cell models of DCM. The cardiomyocyte hypertrophy and interstitial fibrosis were attenuated by 6\u2010G treatment in vivo and resulted in an improved heart function. 6\u2010G inhibited the expression of ferroptosis\u2010related protein FACL4 and the content of iron and enhanced the expression of anti\u2010ferroptosis\u2010related protein GPX4. In addition, 6\u2010G also diminished the secretion of inflammatory cytokines, including IL\u20101<jats:italic>\u03b2<\/jats:italic>, IL\u20106, and TNF\u2010<jats:italic>\u03b1<\/jats:italic>. 6\u2010G treatment activated the Nrf2\/HO\u20101 pathway, enhanced antioxidative stress capacity proved by increased activity of SOD, and decreased MDA production. Compared with in vivo, 6\u2010G treatment of H9c2 cells treated with high glucose and palmitic acid could produce a similar effect. <jats:italic>Conclusion<\/jats:italic>. These findings suggest that 6\u2010G could protect against DCM by the mechanism of ferroptosis inhibition and inflammation reduction via enhancing the Nrf2\/HO\u20101 pathway.<\/jats:p>","DOI":"10.1155\/2022\/3027514","type":"journal-article","created":{"date-parts":[[2023,1,1]],"date-time":"2023-01-01T04:05:06Z","timestamp":1672545906000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":134,"title":["6\u2010Gingerol Alleviates Ferroptosis and Inflammation of Diabetic Cardiomyopathy via the Nrf2\/HO\u20101 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