Estrogen induces cardioprotection in male C57BL/6J mice after acute myocardial infarction via decreased activity of matrix metalloproteinase-9 and increased Akt-Bcl-2 anti-apoptotic signaling
Affiliations: Department of Cardiology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, P.R. China, Department of Cardiology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 197 Rui Jin Road II, Shanghai 200025, P.R. China
- Published online on: April 20, 2011 https://doi.org/10.3892/ijmm.2011.681
- Pages: 231-237
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In general, young men have a greater risk than age-matched women for many types of cardiovascular diseases, including ischemic heart diseases, such as acute or chronic myocardial infarction (MI)-induced heart failure. The effects of estrogen-replacement therapy in men have not been extensively studied. We evaluated the cardioprotective effects of supplemental estrogen against left anterior descending coronary ligation-induced MI in male C57BL/6J mice. A significantly lower prevalence of cardiac rupture was observed in estrogen-treated mice regardless of castration status. A reduced prevalence of cardiac rupture was associated with decreased activities of matrix metalloproteinase 9 (MMP-9) and increased expression of the anti-apoptotic gene Bcl-2. In vitro studies using H9C2 cells under simulated ischemia re-oxygenation treatment further support the role of estrogen receptor β in estrogen-mediated cardioprotection through the Akt-Bcl-2 signaling pathway.