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

Abstract

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−1·d−1) for 30 days; groups III and IV: rats orally received MTK at 10 and 20 mg·kg−1·d−1, 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−1). 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.

Potential Effects of Boldine on Oxidative Stress, Apoptosis, and Inflammatory Changes Induced by the Methylprednisolone Hepatotoxicity in Male Wistar Rats

“…In the MPL-treated group, hepatic LPO and NOx levels were significantly higher, while GSH level was significantly lower, when compared to the control group. These results agree with previous findings by Hegab et al 51 where an imbalance in redox status was observed after prednisolone administration, with significant higher levels of hepatic LPO and reduced levels of antioxidant enzymes. This could be related to an increase in ROS caused by mitochondrial dysfunction cytochrome P450 isoforms induction by prednisolone.…”

Montelukast Prevents Mice Against Acetaminophen-Induced Liver Injury

“…Several studies investigated that montelukast has an antioxidant effect in intestinal ischemia–reperfusion injury (Wu et al, 2015) and also reduces cardiac damage (Khodir et al, 2016). The beneficial effects of montelukast have also been reported in various experimental models of liver injury (El-Boghdady et al, 2017; Hegab et al, 2018). However, the mechanism of montelukast in APAP-induced hepatotoxicity remains unknown.…”

Montelukast modifies simvastatin‐induced myopathy and hepatotoxicity

“…In previous studies, MNK had some hepatoprotective effects against acetaminophen-induced liver injury ( _ lçer et al, 2016), experimentalinduced obstructive jaundice (Kuru et al, 2015), prednisolone-induced liver injury (Hegab, El-Horany, Elbatsh, & Helal, 2018), and paraquateinduced liver injury (El-Boghdady, Abdeltawab, & Nooh, 2017). MNK has also some protective effects on skeletal muscles in an ischemia reperfusion injury (IRI) model (Bilgiç, Altun, Çakıcı, Gidero glu, & Saka, 2018).…”