The protective potential of alpha lipoic acid on amiodarone-induced pulmonary fibrosis and hepatic injury in rats

• Published in: Molecular and cellular biochemistry Vol. 476; no. 9; pp. 3433 - 3448
• Main Authors: Ibrahim Fouad, Ghadha, R. Mousa, Mohamed
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.09.2021; Springer; Springer Nature B.V
• Subjects: Actin; Alanine; Amiodarone; Antioxidants; Aspartate; Biochemistry; Biological response modifiers; Biomedical and Life Sciences; Cardiology; Cholesterol; Fibrosis; Glutathione; Growth factors; Hepatotoxicity; Hydroxyproline; Inflammation; Interferon; Life Sciences; Lipoic acid; Liver; Lung diseases; Lungs; Malondialdehyde; Medical Biochemistry; Muscle proteins; Muscles; Oncology; Oxidants; Oxidative stress; Oxidizing agents; Pulmonary fibrosis; Rodents; Serum levels; Smooth muscle; Transaminase; Transaminases; Transforming growth factor-b1; Transforming growth factors; γ-Interferon; Amiodarone; Pulmonary fibrosis; Alpha lipoic acid; Hepatotoxicity; Hydroxyproline; Transforming growth factor beta-1 (TGF-β1)
• ISSN: 0300-8177; 1573-4919
• DOI: 10.1007/s11010-021-04173-7

Amiodarone (AMD) is a widely used antiarrhythmic drug prescribed to treat cardiac tachyarrhythmias; however, AMD has been reported to provoke pulmonary fibrosis (PF) and hepatotoxicity. This study aimed to investigate the influence of alpha lipoic acid (ALA) on AMD-induced PF and hepatotoxicity in male Wistar rats. AMD administration resulted in elevated lung contents of hydroxyproline (Hyp), malondialdehyde (MDA), and increased serum levels of transforming growth factor beta-1 (TGF-β1), interferon-γ (IFN-γ), alanine amino transaminase (ALT), aspartate amino transaminase (AST), total cholesterol (TC), and glucose. On the other side, lung content of glutathione reduced (GSH) and serum levels of total anti-oxidant capacity (TAC) were significantly decreased. Histopathologically, AMD caused PF, produced a mild hepatic injury, and increased expression of alpha smooth muscle actin (α-SMA). Treatment with ALA produced a significant reversal of the oxidative stress, fibrosis, and inflammation parameters with reductions in α-SMA expressions, leading to amelioration of histopathological lesions. ALA might provide supportive therapy in AMD-receiving cardiovascular patients.