Effect of Montelukast and MK-886 on Hepatic Ischemia-Reperfusion Injury in Rats

Dağlar, Gül; Karaca, Turgut; Yüksek, Yunus Nadi; Gözalan, Uğur; Akbıyık, Filiz; Sökmensüer, Cenk; Gürel, Bora; Kama, Nuri Aydın

doi:10.1016/j.jss.2008.02.052

Cited by 43 publications

(36 citation statements)

References 30 publications

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“…[16] In another trial focusing on the liver, it was demonstrated that montelukast reversed the histopathological alterations and protected from the tissue from damage due to I/R injury. [17] The results were similar both in kidney and bladder tissues, and the protective effects of montelukast have been proven. [9,10] Montelukast has also been studied previously in testicular torsion models.…”

Section: Discussionmentioning

confidence: 55%

Montelukast prevents testes against ischemia-reperfusion injury through suppression of iNOS expression

Sılay

Toklu

Ozagari

et al. 2014

Turkish Journal of Urology

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Objective: To elucidate the mechanism of a possible protective effect of montelukast against testicular ischemia/reperfusion (I/R) injury. Material and methods:Fifty-one adult male Wistar-Albino rats were randomly assigned into 6 groups; sham + saline (S), sham + montelukast (M), I/R + S, I/R + S 30', I/R + M and I/R + M 30'. Saline or montelukast (10 mg/kg) was intraperitoneally administered 30 minutes prior to (S 30', M 30') and during detorsion (I/R + S, I/R + M) in the I/R groups. The I/R groups underwent 2 hours of ischemia followed by 4 hours (early-term) of reperfusion in unilateral testes. Half of the rats underwent 24 hours (late-term) of reperfusion to investigate long-term effects. Testicular tissue samples were examined for biochemical and histopathological parameters. Germ cell apoptosis was evaluated using apoptosis-activating factor 1 (Apaf-1). Inducible nitric oxide synthase (iNOS) activity was analyzed in late-term reperfusion groups. Spermatogenic functions were assessed for each testis based on the Johnsen criteria.Results: Unilateral I/R caused a significant increase in serum TNF-α levels in the early-term group compared to the sham groups. Malondialdehyde levels and myeloperoxidase activity were found to be elevated in the I/R groups and accompanied with a significant decrease in glutathione levels when compared to the sham groups. I/R significantly increased iNOS activity and germ cell apoptosis compared to the sham groups. Montelukast treatment significantly reversed all of these parameters and achieved comparable results with the sham groups. Finally, spermatogenic indices were similar for the bilateral testes between all groups. Conclusion:Montelukast exerts protective effects against testicular I/R injury by inhibiting neutrophil activity, reversing the oxidative stress markers, decreasing iNOS activity and attenuating apoptosis.

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Section: Discussionmentioning

confidence: 55%

Montelukast prevents testes against ischemia-reperfusion injury through suppression of iNOS expression

Sılay

Toklu

Ozagari

et al. 2014

Turkish Journal of Urology

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“…Hydrazine is an oxidant that is known to cause liver injury, including loss of functional integrity of cell membranes in liver tissue 5,38 . AST and ALT are released into the blood following liver damage, thus they have been used as biomarkers of hepatic damage 26,30,39 .…”

Section: Discussionmentioning

confidence: 99%

Characterization of melanin extracted from apricot (Armeniaca sibirica) and its effect on hydrazine-induced rat hepatic injury

Li¹,

Li²,

Zhao³

2016

ScienceAsia

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ABSTRACT:Melanin is a complex, highly coloured natural antioxidant with potent biological activities and diverse applications. A potential source of melanin is the Siberian apricot (Armeniaca sibirica) whose kernel skin is currently a waste by-product. To explore its potential, melanin from apricot kernel skin was extracted. The molecular mass was determined by gel chromatography and its structure was examined by elemental analysis, UV-Vis, infrared, and solid-state nuclear magnetic resonance ( 13 C-NMR) spectroscopy. In addition, its protective effect against hydrazineinduced hepatic injury in rats was evaluated. The results showed that melanin has < 5% sulphur (S) content, indicating that it consists mostly of eumelanin. Its UV-Vis, infrared and 13 C-NMR spectra were very similar to those of synthetic melanin, although it had relatively high carboxylate, aliphatic, and phenol-skeleton content. Two distinct fractions (2.4 ± 0.12 and 0. ± 560.1 kDa) were detected. Injections of hydrazine at 65 mg/kg body-weight (b.wt.) doses resulted in significant (p < 0.01) increases in lipid peroxidation (malondialdehyde contents) in liver homogenates and serum alanine aminotransferase and aspartate aminotransferase activities (64%, 69%, and 98% increase relative to the controls, respectively). It also induced significant (p < 0.05 or 0.01) decreases in liver homogenate catalase, glutathione peroxidase, and superoxide dismutase activities and reduced glutathione content (48%, 28%, 7%, and 98% reduction, respectively). Administering melanin prior to hydrazine, at 10 mg/kg b.wt., strongly inhibited these changes and ameliorated histopathological hepatic injury. The results indicated that melanin alleviated hydrazine-induced liver injury by relieving oxidative stress, which may provide a novel protective strategy for protection against liver diseases.

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“…In I/R injury, ROS exert a central role in the injury of cellular membranes leading to lipid peroxidation in ischemic organs (Daglar et al 2009). Endothelial cells, as well as Kupffer cells, primarily generate oxygen radicals by NADPH oxidase after hepatic I/R.…”

Section: Discussionmentioning

confidence: 99%

“…MDA, which is one of the stable end-products of lipid peroxides, is produced from cell membrane destruction by oxygen radicals. Therefore, MDA is considered as a marker of oxygen radicals and lipid peroxidation of endothelial cells (Nakano et al 2009) or a sensitive index to assess lipid peroxidation (Daglar et al 2009). …”

Section: Discussionmentioning

confidence: 99%

“…Hepatic ischemia/reperfusion (I/R) injury is an important pathological process leading to systemic and hepatic damage after circulatory shock, hepatic trauma, transplantation or hepatic surgery (Daglar et al 2009). I/R injury is a result of a series of complex mechanisms including free oxygen radicals activated by energy depletion and failure of oxygen delivery to the vital tissues in the ischemic period (Yaylak et al 2008).…”

Section: Introductionmentioning

confidence: 99%

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Preventive role of gallic acid on hepatic ischemia and reperfusion injury in rats

et al. 2014

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There is little information about the hepatoprotective effects of gallic acid against ischemiareperfusion (I/R) damage. Animals were subjected to I/R. Gallic acid at doses of 50 and 100 mg/kg body weight (bw) were injected as a single dose prior to ischemia. Liver tissue homogenates were used for the measurement of malondialdehyde (MDA), catalase (CAT) and glutathione peroxidase (GPx) levels. At the same time alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) were assayed in serum samples and compared statistically. While the ALT, AST, LDH activities and MDA levels were significantly increased, CAT and GPx activities significantly decreased in only I/Rinduced control rats compared to normal control rats (P \ 0.05). Treatment with gallic acid at a dose of 100 mg/kg bw significantly decreased the ALT, AST, LDH activities and MDA levels, and markedly increased activities of CAT and GPx in tissue homogenates compared to I/R-induced rats with no treatment group (P \ 0.05). In oxidative stress generated by hepatic ischemia-reperfusion, gallic acid contributes partially an alteration in the delicate balance between the scavenging capacity of antioxidant defense systems and free radicals in favour of the antioxidant defense systems in the body.

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Effect of Montelukast and MK-886 on Hepatic Ischemia-Reperfusion Injury in Rats

Cited by 43 publications

References 30 publications

Montelukast prevents testes against ischemia-reperfusion injury through suppression of iNOS expression

Montelukast prevents testes against ischemia-reperfusion injury through suppression of iNOS expression

Characterization of melanin extracted from apricot (Armeniaca sibirica) and its effect on hydrazine-induced rat hepatic injury

Preventive role of gallic acid on hepatic ischemia and reperfusion injury in rats

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