Gallic acid attenuates pulmonary fibrosis in a mouse model of transverse aortic contraction-induced heart failure |
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| Affiliation: | 1. Heart Research Center of Chonnam National University Hospital, Gwangju 501-757, Republic of Korea;2. Jilin Hospital Affiliated with Jilin University, 4 Nanjing street, Chuanying, Jilin 132011, China;3. The Second Hospital of Jilin University, Changchun, Jilin 130041, China;4. Department of Forensic Medicine, Chonnam National University Medical School, Gwangju, Republic of Korea;1. Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, PR China;2. Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei Province, PR China;3. Department of Cardiology, The First Affiliated Hospital of Yangtze University, Jingzhou, PR China;1. Signalisation et Physiopathologie Cardiovasculaire, UMR-S 1180, Univ. Paris-Sud, INSERM, Université Paris-Saclay, Châtenay-Malabry 92296, France;2. Univ. Paris–Sud, Faculté de Médecine, Université Paris-Saclay, Le Kremlin Bicêtre, France;3. Assistance Publique Hôpitaux de Paris, Service de Pneumologie, Hôpital Bicêtre, Le Kremlin Bicêtre, France;4. Inserm UMR_S 999, Hôpital Marie Lannelongue, Le Plessis Robinson, France |
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| Abstract: | Gallic acid, a trihydroxybenzoic acid found in tea and other plants, attenuates cardiac hypertrophy, fibrosis, and hypertension in animal models. However, the role of gallic acid in heart failure remains unknown. In this study, we show that gallic acid administration prevents heart failure-induced pulmonary fibrosis. Heart failure induced in mice, 8 weeks after transverse aortic constriction (TAC) surgery, was confirmed by echocardiography. Treatment for 2 weeks with gallic acid but not furosemide prevented cardiac dysfunction in mice. Gallic acid significantly inhibited TAC-induced pathological changes in the lungs, such as increased lung mass, pulmonary fibrosis, and damaged alveolar morphology. It also decreased the expression of fibrosis-related genes, including collagen types I and III, fibronectin, connective tissue growth factor (CTGF), and phosphorylated Smad3. Further, it inhibited the expression of epithelial-mesenchymal transition (EMT)-related genes, such as N-cadherin, vimentin, E-cadherin, SNAI1, and TWIST1. We suggest that gallic acid has therapeutic potential for the treatment of heart failure-induced pulmonary fibrosis. |
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