Amiodarone (AD) is one of the most frequently prescribed anti-arrhythmic agents worldwide, but its effectiveness is
limited due to the development of pulmonary toxicity. Several lines of evidence have suggested that AT1 receptor antagonists
can attenuate pulmonary fibrosis in different animal models. This study was performed to evaluate the effect of olmesartan
medoxomil (OM) on lung injury induced in rats by AD which was assessed biochemically (hydroxyproline content, MDA level
and SOD activity), histologically (Ashcroft criteria and Masson’s trichrome stain) and immunohistochemically (TGF-b1 expression
in lung tissue). The expression levels of TGF-b1 and type I collagen mRNA were also determined by quantitative real-time
polymerase chain reaction. Forty-eight adult male rats were randomized into six equal groups: control group, OM control groups,
AD group received 40 mg/kg/day, p.o. for 4 weeks to induce pulmonary injury in rats and OM-treated groups received 0.6 and
6 mg/kg/day, p.o. concomitantly with AD for the same period. The results indicated that OM significantly decreased collagen
deposition and hydroxyproline content, ameliorated pathological score and decreased the elevation in type I collagen and TGFß1
mRNA expression in lung tissue. Furthermore, it attenuated the AD-induced increase in the MDA level and increased SOD
activity in lung tissue. It can be concluded that OM exerts a protective effect against AD-induced lung damage in rats which is
attributed to modulation of pro-fibrogenic cytokine (TGF-b1) and antioxidant effect.