Protocatechuic acid reverses myocardial infarction mediated by β-adrenergic agonist via regulation of Nrf2/HO-1 pathway,inflammatory, apoptotic,and fibrotic events |
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Authors: | Li Li Hua Ma Yichong Zhang Haitao Jiang Bihua Xia Hassan Al Sberi Mohamed A Elhefny Maha S Lokman Rami B Kassab |
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Institution: | 1. Department of Cardiology, HenanProvincial Chest Hospital, Zhengzhou University, Zhengzhou City, Henan Province, 450000 China;2. Department of Vasculocardiology, Xianyang Central Hospital, Xianyang, China;3. Department of Internal Medicine, The Second Affiliated Hospital of Xinxiang Medical College, Xinxiang City, Henan Province, China;4. Department of Cardiology, Chifeng Municipal Hospital, Chifeng City, China;5. The First Department of Cardiology, The Second Affiliated Hospital of GuiZhou Medical University, Kaili City, Guizhou Province, China;6. Basic Medical Science, Histopathology Department, National Organization for Drug Control and Research, Giza, Egypt
Department of Biology, Faculty of Science, Taif University, Taif, Saudi Arabia;7. Department of Cancer and Molecular Biology, National Cancer Institute, Cairo University, Cairo, Egypt
Department of Medical Genetics, Faculty of Medicine, Umm Al-Qura University, Alqunfudah, Saudi Arabia;8. Department of Biology, College of Science and Humanities in Al-Kharj, Prince Sattam Bin Abdulaziz University, Al-kharj, Saudi Arabia;9. Department of Zoology and Entomology, Faculty of Science, Helwan University, Cairo, Egypt
Department of Biology, Faculty of Science and Arts, Al-Baha University, Almakhwah, Al-Baha, Saudi Arabia |
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Abstract: | Myocardial infarction (MI) is an instant ischemic death of cardiomyocytes that remains a major global cause of mortalities. MI is accompanied by oxidative, inflammatory, apoptotic, and fibrotic insults. Protocatechuic acid (PCA) is a polyphenolic compound with various potent biological activities. In this study, we explored the possible cardioprotective role of PCA against isoproterenol (ISO)-mediated MI. Rats were either injected with ISO (85 mg/kg, subcutaneously) or pretreated with PCA (100 or 200 mg/kg, orally). PCA supplementation markedly normalized ISO-induced disturbed cardiac function markers (creatine kinase-MB, lactate dehydrogenase, and troponin T). Notably, PCA administration exerted remarkable increases in glutathione and its derived enzymes, superoxide dismutase, and catalase, as well as decreases in malondialdehyde and nitric oxide levels in the injured cardiac tissue. The molecular findings validated the augmented cellular antioxidative capacity by PCA via increasing the gene expressions of nuclear factor erythroid 2-related factor 2 and heme oxygenase-1. The cardioprotective efficacy of PCA extended to suppress cardiac inflammation as demonstrated by the decreased levels of tumor necrosis factor-alpha, interleukin-1 beta, and nuclear factor kappa B. Additionally, PCA prevented cardiomyocyte loss and fibrosis by decreasing Bax, caspase-3, transforming growth factor-β1 and matrix metalloproteinase-9, and enhancing B-cell lymphoma 2 and tissue inhibitors of metalloproteinase-3. The cardiac histological screening further confirmed the PCA's protective action. The obtained data recommend PCA as an alternative therapeutic agent to attenuate the molecular, biochemical, and histological alterations associated with MI development. |
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Keywords: | apoptosis fibrosis inflammation myocardial infarction oxidative insult protocatechuic acid |
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