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        Ferulic acid protects cardiomyocytes from TNF-a/cycloheximide-induced apoptosis by regulating autophagy

        Chunxiao Li,Lu Chen,Min Song,Zhirui Fang,Lusha Zhang,Joel Wake Coffie,Liyuan Zhang,Lulu Ma,Qianyi Wang,Wenjie Yang,Leyu Fang,Shaoxia Wang,Xiumei Gao,Hong Wang 대한약학회 2020 Archives of Pharmacal Research Vol.43 No.8

        Acute myocardial infarction (AMI) resultsin irreversible cardiac cell damage or death because ofdecreased blood fl ow to the heart. Apoptosis plays an importantrole in the process of tissue damage after myocardialinfarction (MI), which has pathological and therapeuticimplications. Ferulic acid (FA) is a phenolic acid endowedwith strong antioxidative and cytoprotective activities. Thepresent study aimed to investigate whether FA protectscardiomyocytes from apoptosis by regulating autophagy,which is a cellular self-digestion process, and one of thefi rst lines of defense against oxidative stress. Apoptosis wasinduced by TNF-α (10 ng/mL) and cycloheximide (CHX,5 μg/mL) in rat H9c2 cardiomyocytes. FA-inhibited TNF-α/CHX-induced apoptosis was determined by the quantifi cationof TUNEL-positive cells, and the eff ect was associatedwith decreased ROS production and inhibited caspase3activation. FA treatment enhanced autophagy and increasedautophagy-associated protein expression, leading to an inhibitionof mTOR signaling. When co-treated with 3-methyladenine(3-MA), an autophagy inhibitor, the anti-apoptoticeff ect of FA was attenuated. In an in vivo mouse MI model,FA treatment decreased the apoptotic cell number, reducedinfarct size, and improved cardiac performance, as determinedby histological and echocardiographic assessments. Taken collectively, these results suggest that FA could protectcardiomyocytes from apoptosis by enhancing autophagy.

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