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Year : 2014  |  Volume : 10  |  Issue : 38  |  Page : 132-140

Effect of Aronia melanocarpa fruit juice on amiodarone-induced pneumotoxicity in rats

1 Department of Preclinical and Clinical Pharmacology and Toxicology, Medical University, Varna, Bulgaria
2 Department of Experimental and Clinical Pharmacology, Medical University, Pleven, Bulgaria
3 Department of Disaster Medicine, Medical University, Pleven, Bulgaria
4 Department of Clinical Laboratory, Clinical Immunologyand Allergology, Clinic of Allergology, University Hospital, Pleven, Bulgaria
5 Department of Biology, Medical University, Pleven, Bulgaria
6 Department of Chemistry, Medical University, Pleven, Bulgaria
7 Department of Physiology and Pathophysiology, Medical University, Pleven, Bulgaria

Correspondence Address:
Stefka Valcheva-Kuzmanova
Department of Preclinical and Clinical Pharmacology and Toxicology, Medical University, 55, Marin Drinov Str.,9002 Varna
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0973-1296.131024

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Background: The fruits of Aronia melanocarpa (Michx.) Elliot is extremely rich in biologically active polyphenols. Objective: We studied the protective effect of A. melanocarpa fruit juice (AMFJ) in a model of amiodarone (AD)-induced pneumotoxicity in rats. Materials and Methods: AD was instilled intratracheally on days 0 and 2 (6.25 mg/kg). AMFJ (5 mL/kg and 10 mL/kg) was given orally from day 1 to days 2, 4, 9, and 10 to rats, which were sacrificed respectively on days 3, 5, 10, and 28 when biochemical, cytological, and immunological assays were performed. Results: AMFJ antagonized AD-induced increase of the lung weight coefficient. In bronchoalveolar lavage fluid, AD increased significantly the protein content, total cell count, polymorphonuclear cells, lymphocytes and the activity of lactate dehydrogenase, acid phosphatase and alkaline phosphatase on days 3 and 5. In AMFJ-treated rats these indices of direct toxic damage did not differ significantly from the control values. In lung tissue, AD induced oxidative stress measured by malondialdehyde content and fibrosis assessed by the hydroxyproline level. AMFJ prevented these effects of AD. In rat serum, AD caused a significant elevation of interleukin IL-6 on days 3 and 5, and a decrease of IL-10 on day 3. In AMFJ-treated rats, these indices of inflammation had values that did not differ significantly from the control ones. Conclusion: AMFJ could have a protective effect against AD-induced pulmonary toxicity as evidenced by the reduced signs of AD-induced direct toxic damage, oxidative stress, inflammation, and fibrosis.

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