{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,29]],"date-time":"2026-07-29T05:03:02Z","timestamp":1785301382696,"version":"3.55.0"},"reference-count":35,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2023,7,8]],"date-time":"2023-07-08T00:00:00Z","timestamp":1688774400000},"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":["J Biochem &amp; Molecular Tox"],"published-print":{"date-parts":[[2023,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Acute myocardial infarction is regarded as myocardial necrosis resulting from myocardial ischemia\/reperfusion (I\/R) damage and retains a major cause of mortality. Neferine, which was extracted from the green embryos of mature seeds of <jats:italic>Nelumbo nucifera<\/jats:italic>\u00a0Gaertn., has been reported to possess a broad range of biological activities. However, its underlying mechanism on the protective effect of I\/R has not been fully clarified. A hypoxia\/reoxygenation (H\/R) model with H9c2 cells closely simulating myocardial I\/R injury was used as a cellular model. This study intended to research the effects and mechanism underlying neferine on H9c2 cells in response to H\/R stimulation. Cell Counting Kit\u20108 and lactate dehydrogenase\u00a0(LDH) release assays were employed to measure cell viability and LDH, respectively. Apoptosis and reactive oxygen species (ROS) were determined by flow cytometry analysis. Oxidative stress was evaluated by detecting malondialdehyde, superoxide dismutase,\u00a0and catalase. Mitochondrial function was assessed by mitochondrial\u00a0membrane potential, ATP content, and mitochondrial ROS. Western blot analysis was performed to examine the expression of related proteins. The results showed that hypoxia\/reoxygenation (H\/R)\u2010induced cell damage, all of which were distinctly reversed by neferine. Moreover, we observed that neferine inhibited oxidative stress and mitochondrial dysfunction induced by H\/R in H9c2 that were concomitant with increased sirtuin\u20101\u00a0(SITR1), nuclear factor erythroid 2\u2010related factor 2 (Nrf2), and heme oxygenase\u20101\u00a0expression. On the contrary, silencing the SIRT1 gene with its small interferingRNA eliminated the beneficial effects of neferine. It is concluded that neferine preconditioning attenuated H\/R\u2010induced cardiac damage via suppressing apoptosis, oxidative stress, and mitochondrial dysfunction, which may be partially ascribed to the activation of SIRT1\/Nrf2 signaling pathway.<\/jats:p>","DOI":"10.1002\/jbt.23398","type":"journal-article","created":{"date-parts":[[2023,7,8]],"date-time":"2023-07-08T10:09:48Z","timestamp":1688810988000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Neferine protected cardiomyocytes against hypoxia\/oxygenation injury through SIRT1\/Nrf2\/HO\u20101 signaling"],"prefix":"10.1002","volume":"37","author":[{"given":"Cheng","family":"Lu","sequence":"first","affiliation":[{"name":"Department of Cardiology Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine Shanghai 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