The effect of montelukast on bronchial hyperreactivity and lung function in asthmatic children aged 6-13 years.

Background: Cysteinyl leukotrienes have been shown to play an important role in the pathogenesis of asthma. The effect of the leukotriene receptor antagonist, montelukast, on bronchial hyperreactivity (BHR) as measured by the methacholine challenge test in school children has not been reported. Objective: To determine the effect of montelukast (Singulairâ) on BHR measured by methacholine challenge and lung function tests in Thai asthmatic children aged 6-13 years. Materials and methods: This was a randomized, double-blind, placebo-controlled, crossover study performed in 29 mild to moderate persistent asthmatic children aged 6-13 years. Each child received crossover treatment with 6 weeks of montelukast (5 mg/day) and 6 weeks of placebo separated by a two-week washout period. Results: The improvement of FEV1 and FEV1/FVC after 6 weeks of treatment was significantly higher in montelukast group compared to those of placebo group (p<0.05). After 6 weeks of treatment, mean (+ SEM) PC was 20 in the placebo group (5.7 + 1.41 mg/ml) which was lower than in montelukast group (6.8 + 1.74 mg/ml) but there was no significant difference (p=0.79). Conclusion: Montelukast significantly improved FEV1 and FEV1/FVC but not BHR in mild to moderate persistent asthmatic children aged 6-13 years after the 6 weeks of treatment.

Therapeutic effect of pranlukast, a cysteinyl leukotriene receptor antagoist, on focal cerebral ischemia in mice / 中国药理学通报

Aim To determine whether pranlukast (ONO-1078), a cysteinyl leukotriene receptor antagonist, possesses therapeutic effect when administered after focal cerebral ischemia in mice. Methods Persistent focal cerebral ischemia was induced by middle cerebral artery occlusion. Pranlukast and edaravone, a positive control drug, were ip injected 1, 6 and 24 h after ischemia. The neurological deficits were evaluated by neurological scores and inclined plane test 24 and 48 h after the surgery. Forty-eight h later, the brain slices were prepared for measurements of infarct volume and the ratio of ischemic/non-ischemic hemispheres. Brain sections were cut and examined for neuron densities in different regions of the brain. The effects of pranlukast and edaravone were evaluated by the changes of these variables. Results Pranlukast (0.1 and 0.2 mg?kg -1) and edaravone (3 and 10 mg?kg -1) significantly reduced the neurological deficits, infarct volume (maximally 82.3%), ratio of ischemic/non-ischemic hemispheres, and attenuated the reduction of neuron densities in hippocampal CA1 region, cortex and striatum. Conclusion Pranlukast possesses therapeutic effect on ischemic insults when administered after ischemia as effective as edravone, indicating a therapeutic potential in the treatment of ischemic stroke.