Montelukast abrogates prednisolone-induced hepatic injury in rats: Modulation of mitochondrial dysfunction, oxidative/nitrosative stress, and apoptosis.

The aim of this study was to investigate the protective effect of montelukast (MTK) against prednisolone-induced hepatic injury in rats. Twenty-eight male albino rats were categorized into four equal groups. Group I served as the control group; group II: rats orally received prednisolone (5 mg·kg ·d ) for 30 days; groups III and IV: rats orally received MTK at 10 and 20 mg·kg ·d , respectively, simultaneously with prednisolone for 30 days. Serum liver enzymes, hepatic mitochondrial function, oxidative/nitrosative stress, and inflammatory and apoptotic markers were evaluated, and the results were confirmed by histopathological examination. MTK showed significant hepatic protection evidenced by alleviated histological lesion and improvement of mitochondrial function, oxidative/nitrosative stress, and inflammatory and apoptotic changes induced by prednisolone, with more profound protection in higher MTK dose (20 mg·kg ). In view of these findings, we can conclude that MTK may have hepatoprotective potential, beyond its therapeutic value for asthmatic patients during their course of corticosteroid therapy.