Ferulic acid protects cardiomyocytes from TNF-α/cycloheximide-induced apoptosis by regulating autophagy
| Autor: | Lusha Zhang, Leyu Fang, Shaoxia Wang, Lulu Ma, Xiumei Gao, Wenjie Yang, Qianyi Wang, Liyuan Zhang, Lu Chen, Joel Wake Coffie, Hong Wang, Min Song, Zhirui Fang, Chunxiao Li |
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| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Male Coumaric Acids Myocardial Infarction Apoptosis Cycloheximide Pharmacology medicine.disease_cause Cell Line Ferulic acid 03 medical and health sciences chemistry.chemical_compound Mice 0302 clinical medicine In vivo Drug Discovery medicine Autophagy Animals Myocytes Cardiac Myocardial infarction Tumor Necrosis Factor-alpha Adenine Organic Chemistry Phenolic acid medicine.disease Rats Mice Inbred C57BL Disease Models Animal Oxidative Stress 030104 developmental biology chemistry 030220 oncology & carcinogenesis Molecular Medicine Reactive Oxygen Species Oxidative stress |
| Zdroj: | Archives of pharmacal research. 43(8) |
| ISSN: | 1976-3786 |
| Popis: | Acute myocardial infarction (AMI) results in irreversible cardiac cell damage or death because of decreased blood flow to the heart. Apoptosis plays an important role in the process of tissue damage after myocardial infarction (MI), which has pathological and therapeutic implications. Ferulic acid (FA) is a phenolic acid endowed with strong antioxidative and cytoprotective activities. The present study aimed to investigate whether FA protects cardiomyocytes from apoptosis by regulating autophagy, which is a cellular self-digestion process, and one of the first lines of defense against oxidative stress. Apoptosis was induced 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 quantification of TUNEL-positive cells, and the effect was associated with decreased ROS production and inhibited caspase3 activation. FA treatment enhanced autophagy and increased autophagy-associated protein expression, leading to an inhibition of mTOR signaling. When co-treated with 3-methyladenine (3-MA), an autophagy inhibitor, the anti-apoptotic effect of FA was attenuated. In an in vivo mouse MI model, FA treatment decreased the apoptotic cell number, reduced infarct size, and improved cardiac performance, as determined by histological and echocardiographic assessments. Taken collectively, these results suggest that FA could protect cardiomyocytes from apoptosis by enhancing autophagy. |
| Databáze: | OpenAIRE |
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