Cysteinyl leukotriene receptor antagonist montelukast ameliorates acute lung injury following haemorrhagic shock in rats†

Al-Amran, Fadhil G.; Hadi, Najah R; Hashim, Ali M.

doi:10.1093/ejcts/ezs312

Cited by 30 publications

(20 citation statements)

References 28 publications

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“…It is widely used as antiasthmatic therapy for chronic asthma and seasonal allergies with high tolerability in both children and adults [41,42]. It was tested for various pathological conditions as spinal cord injury [43], hippocampal ischemia [44], and hemorrhagic shock [45]. A few years ago, it attracted scientists to be evaluated as a protection for various toxic agents.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Montelukast against Cadmium Induced Pituitary Gland Toxicity

Ek¹,

Mf²,

Mg³

et al. 2017

IJCPT

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Adult male Sprague rats weighting (220 ± 30gm) were purchased from Faculty of Agriculture, Minia University Egypt. Experimen- AbstractCadmium (Cd) is a common environmental hazardous heavy metal. The standard treatment of heavy metal intoxication; chelators may have a minor role in Cd toxicity. Montelukast (ML) is an anti-inflammatory drug that is used mainly for managing asthmatic patients. Recent workers have tested ML for its antioxidant properties in various conditions and obtained encouraging results as regarding this effect. We investigated the protective and antioxidant effect of ML on pituitary gland, a highly sensitive organ to Cd toxicity. Four groups of rats were used and received distilled water, 10mg/kg ML, 3mg/kg Cd, and 10mg ML plus 3mg/kg Cd respectively. Antioxidant, histological, immunohistochemical and hormonal effects of Cd and ML were evaluated. The detrimental effect of Cd on pituitary gland was abolished by ML. The diminished hormonal effect of Cd was restored to normal levels. The increased MDA level and depleted oxidative enzymes on pituitary gland of rat exposed to Cd were restored by ML. lastly, histological and apoptotic effects of Cd were also, corrected significantly by ML. It is concluded that ML can protect against Cd-induced pituitary gland toxicity.

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Section: Discussionmentioning

confidence: 99%

Protective Effect of Montelukast against Cadmium Induced Pituitary Gland Toxicity

Ek¹,

Mf²,

Mg³

et al. 2017

IJCPT

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“…Indeed, the blockade of CysLTR1 signaling by montelukast attenuated NIHL, even though we posttreated the mice with montelukast after noise exposure. CysLTR1 antagonists such as montelukast and pranlukast have been reported to protect against ischemia/reperfusion injury in a variety of tissues such as in the heart, liver, kidneys, and spinal cord, and the mechanism of these effects was suspected to involve a decrease in inflammation and oxidative stress (25)(26)(27)(28)(29). As inflammation and oxidative stress are also known to contribute to NIHL, we first explored whether montelukast protected against noise-induced cochlear injury through the regulation of oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Role of cysteinyl leukotriene signaling in a mouse model of noise-induced cochlear injury

Park¹,

Kang²,

Seo

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Noise-induced hearing loss is one of the most common types of sensorineural hearing loss. In this study, we examined the expression and localization of leukotriene receptors and their respective changes in the cochlea after hazardous noise exposure. We found that the expression of cysteinyl leukotriene type 1 receptor (CysLTR1) was increased until 3 d after noise exposure and enhanced CysLTR1 expression was mainly observed in the spiral ligament and the organ of Corti. Expression of 5-lipoxygenase was increased similar to that of CysLTR1, and there was an accompanying elevation of CysLT concentration. Posttreatment with leukotriene receptor antagonist (LTRA), montelukast, for 4 consecutive days after noise exposure significantly decreased the permanent threshold shift and also reduced the hair cell death in the cochlea. Using RNA-sequencing, we found that the expression of matrix metalloproteinase-3 (MMP-3) was up-regulated after noise exposure, and it was significantly inhibited by montelukast. Posttreatment with a MMP-3 inhibitor also protected the hair cells and reduced the permanent threshold shift. These findings suggest that acoustic injury up-regulated CysLT signaling in the cochlea and cochlear injury could be attenuated by LTRA through regulation of MMP-3 expression. This study provides mechanistic insights into the role of CysLTs signaling in noise-induced hearing loss and the therapeutic benefit of LTRA.

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“…Consequently, blocking LT pathways may be beneficial in asthma, and this has led to the development of 5-LO enzyme inhibitors (e.g., zileutin) and CysLT1 receptor antagonists (e.g., montelukast, zafirlukast, and pranlukast) (Barnes, 2011;Peters-Golden and Henderson, 2007). Montelukast has been shown to reduce lung inflammation in animal models (Al-Amran et al, 2012). However, recent meta-analyses have shown that corticosteroids are superior for the treatment of chronic and acute asthma, and the role of these agents in the treatment of asthma remains poorly defined (Chauhan and Ducharme, 2012;Watts and Chavasse, 2012).…”

Section: Leukotrienesmentioning

confidence: 99%

Lipid Mediators and Lung Function

Weinberger

Hirsch

Yin³

et al. 2015

Comparative Biology of the Normal Lung

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Cysteinyl leukotriene receptor antagonist montelukast ameliorates acute lung injury following haemorrhagic shock in rats†

Abstract: The results of the present study reveal that montelukast may ameliorate lung injury in shocked rats by interfering with inflammatory and oxidative pathways, implicating the role of leukotrienes in the pathogenesis of haemorrhagic shock-induced lung inflammation.

Cited by 30 publications

References 28 publications

Protective Effect of Montelukast against Cadmium Induced Pituitary Gland Toxicity

Protective Effect of Montelukast against Cadmium Induced Pituitary Gland Toxicity

Role of cysteinyl leukotriene signaling in a mouse model of noise-induced cochlear injury

Lipid Mediators and Lung Function

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