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Oxid Med Cell Longev. 2018 Jun 25;2018:4327901. doi: 10.1155/2018/4327901. eCollection 2018.

Aucubin Protects against Myocardial Infarction-Induced Cardiac Remodeling via nNOS/NO-Regulated Oxidative Stress.

Yang Z1,2,3, Wu QQ1,2,3, Xiao Y1,2,3, Duan MX1,2,3, Liu C1,2,3, Yuan Y1,2,3, Meng YY1,2,3, Liao HH1,2,3, Tang QZ1,2,3.

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Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Cardiovascular Research Institute, Wuhan University, Wuhan 430060, China.
Hubei Key Laboratory of Cardiology, Wuhan 430060, China.


Whether aucubin could protect myocardial infarction- (MI-) induced cardiac remodeling is not clear. 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 mg/kg) 3 days post-MI. Two weeks post-MI, mice in the aucubin treatment group showed decreased mortality, decreased infarct size, and improved cardiac function. Aucubin also decreased cardiac remodeling post-MI. 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-treated mice heart and in vitro-treated cardiomyocytes, which caused decreased thioredoxin (Trx) consumption, leading to ASK1 forming the inactive complex with Trx. Aucubin increased nNOS-derived NO production in vivo and vitro. The protective effects of aucubin were reversed by the NOS inhibitors L-NAME and L-VINO in vitro. Furthermore, nNOS knockout mice also reversed the protective effects of aucubin on cardiac remodeling. Taken together, aucubin protects against cardiac remodeling post-MI 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.

[Indexed for MEDLINE]
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