Effect of taxifolin on oxidative stress and amiodarone-induced pulmonary toxicity and fibrosis in rats

SÜLEYMAN B., Bilgin A., MAMMADOV R., Cimen F. K., GÜLABOĞLU M.

Latin American Journal of Pharmacy, cilt.37, sa.9, ss.1837-1843, 2018 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 37 Sayı: 9
  • Basım Tarihi: 2018
  • Dergi Adı: Latin American Journal of Pharmacy
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.1837-1843
  • Anahtar Kelimeler: Amiodarone, Lung fibrosis, Oxidative stress, Taxifolin
  • Erzincan Binali Yıldırım Üniversitesi Adresli: Evet

Özet

© 2018, Colegio de Farmaceuticos de la Provincia de Buenos Aires. All rights reserved.Amiodarone, an antiarrhythmic drug, is a benzofuran derivative. Oxidative stress plays a role in the mechanism of amiodarone-induced pulmonary toxicity. Taxifolin has antioxidant and anti-in-flammatory activities. The aim of the study was to investigate the effects of taxifolin on amiodarone-induced pulmonary toxicity in rats. In total 18 male albino Wistar rats were divided into three groups (n = 6 in each group): a taxifolin 50 mg/kg plus amiodarone 30 mg/kg (TAM) group, an amiodarone 30 mg/kg group (AMD) and a healthy group (HG). Malondialdehyde (MDA) levels, total glutathione (tGSH) levels, total oxidant status (TOS) and total antioxidant status (TAS) were measured in lung tissues, and histopathological examinations were performed. MDA and TOS levels in the AMD group were higher than those in the other two groups. In contrast, tGSH and TAS levels in the AMD group were lower than those in the TAM and HG groups. Alveolar destruction, marked oedema, alveolar septal fibrosis, leukocyte infiltration and haemorrhages were seen in the AMD group. Only slight oedema and congestion were observed in the TAM group. Taxifolin may be useful in preventing amiodarone-induced pulmonary toxicity.