الفهرس 
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Abstract
Pulmonary fibrosis takes place as an adverse effect of the class III chemotherapeutic agent, amiodarone (AM), which limits its use as an antiarrhythmic agent. The present study aimed to help in understanding the exact mechanisms as well as to investigate the role of oxidative stress, ATP depletion, apoptosis and inflammatory processes against AM-induced pulmonary fibrosis in rats, to investigate whether thymoquinone (TQ), L-carnitine, or omega-3 can protect against AM-induced pulmonary fibrosis in rats.
In the current study, injection of AM in rats resulted in pulmonary fibrosis. Furthermore, serum α1-antitrypsin, TGF-β1, TNF-α, lactate dehydrogenase, superoxide-dismutase, catalase, glutathione reductase, glutathione peroxidase, reduced glutathione, and malondialdehyde activities were significantly increased in AM-insulted group. Similarly, immunohistochemical staining of tumor necrosis factor-receptor type 1, cytochrome c, caspase-9, cleaved caspase-3 and ssDNA in the lung sections were significantly elevated in AM-insulted group. Treatment with the natural agents TQ, L-carnitine, or omega-3 partially ameliorated most of AM-induced abnormalities indicating their