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In this study, in a mouse model, cardiac remodeling was induced by left anterior descending coronary artery ligation surgery. Mice were intraperitoneally injected with aucubin (10\u2009mg\/kg) 3 days post\u2010MI. Two weeks post\u2010MI, mice in the aucubin treatment group showed decreased mortality, decreased infarct size, and improved cardiac function. Aucubin also decreased cardiac remodeling post\u2010MI. Consistently, aucubin protected cardiomyocytes against hypoxic injury in vitro. Mechanistically, we found that aucubin inhibited the ASK1\/JNK signaling. These effects were abolished by the JNK activator. Moreover, we found that the oxidative stress was attenuated in both in vivo aucubin\u2010treated mice heart and in vitro\u2010treated cardiomyocytes, which caused decreased thioredoxin (Trx) consumption, leading to ASK1 forming the inactive complex with Trx. Aucubin increased nNOS\u2010derived NO production in vivo and vitro. The protective effects of aucubin were reversed by the NOS inhibitors L\u2010NAME and L\u2010VINO in vitro. Furthermore, nNOS knockout mice also reversed the protective effects of aucubin on cardiac remodeling. Taken together, aucubin protects against cardiac remodeling post\u2010MI through activation of the nNOS\/NO pathway, which subsequently attenuates the ROS production, increases Trx preservation, and leads to inhibition of the ASK1\/JNK pathway.<\/jats:p>","DOI":"10.1155\/2018\/4327901","type":"journal-article","created":{"date-parts":[[2018,6,25]],"date-time":"2018-06-25T19:31:58Z","timestamp":1529955118000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":30,"title":["Aucubin Protects against Myocardial Infarction\u2010Induced Cardiac Remodeling via nNOS\/NO\u2010Regulated Oxidative 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