Hemmati, A., Zaeemzadeh, N., Arzi, A., Jalali, T., Rashidi, I. (2011). Protective Effect of Caffeic Acid Phenethyl Ester (CAPE) on Amiodarone-Induced Pulmonary Fibrosis in Rat. Iranian Journal of Pharmaceutical Research, Volume 10(Number 2), 321-328. doi: 10.22037/ijpr.2011.923
A.A. Hemmati; N Zaeemzadeh; A Arzi; T Jalali; I Rashidi. "Protective Effect of Caffeic Acid Phenethyl Ester (CAPE) on Amiodarone-Induced Pulmonary Fibrosis in Rat". Iranian Journal of Pharmaceutical Research, Volume 10, Number 2, 2011, 321-328. doi: 10.22037/ijpr.2011.923
Hemmati, A., Zaeemzadeh, N., Arzi, A., Jalali, T., Rashidi, I. (2011). 'Protective Effect of Caffeic Acid Phenethyl Ester (CAPE) on Amiodarone-Induced Pulmonary Fibrosis in Rat', Iranian Journal of Pharmaceutical Research, Volume 10(Number 2), pp. 321-328. doi: 10.22037/ijpr.2011.923
Hemmati, A., Zaeemzadeh, N., Arzi, A., Jalali, T., Rashidi, I. Protective Effect of Caffeic Acid Phenethyl Ester (CAPE) on Amiodarone-Induced Pulmonary Fibrosis in Rat. Iranian Journal of Pharmaceutical Research, 2011; Volume 10(Number 2): 321-328. doi: 10.22037/ijpr.2011.923
Protective Effect of Caffeic Acid Phenethyl Ester (CAPE) on Amiodarone-Induced Pulmonary Fibrosis in Rat
1Department of Pharmacology and Toxicology, School of Pharmacy, Physiology Research center
2Department of Laboratory Sciences, School of Paramedics
3Department of Pathology, School of Medicine, Ahwaz Jundishapur University of Medical Sciences, Ahwaz, Iran
Abstract
Treatment with amiodarone, a commonly prescribed antidysrhythmic agent, is associated with pulmonary fibrosis (PF) which is a commonly progressive and untreatable dieases. Caffeic acid phenethyl ester (CAPE) is a phenolic antioxidant and an active anti-inflammatory, anticancer, antimicrobial and antioxidant component of propolis (bee glue; a resinous hive product collected by honey bees). In the current study the effects of CAPE on amiodarone-induced pulmonary fibrosis in rat were investigated.
Male rats were divided into 4 groups; first group was received only amiodarone (6.25 mg/kg) on first and third day. The second group received only vehicle (distilled water) with the same volume and time as the first group. Third and fourth groups received amiodarone and treated with CAPE 5 and 10 µmol/kg respectively 2 days before the first dose of amiodarone and 21 days after the second dose of amiodarone. At the end of the course of treatment, lung tissue was removed for histopathology and biochemical evaluations. Malondealdehide (MDA) concentration, myeloperoxidase (MPO) and superoxide dismutase (SOD) activities were determined in lung tissue. Histopathological evaluation was performed using light microscopy.
MDA level and the activity of myeloperoxidase and superoxide dismutase enzymes decreased significantly in the group which was treated with CAPE (5 µmol/kg). However 10 µmol/kg CAPE had not such an effect. Both doses of CAPE could reduce the fibrogenic effects of amiodarone histopathlogically.
In conclusion CAPE was shown to be effective in reducing amiodarone-induced pulmonary fibrosis with the dose of 5 µmol/kg.
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