The cysteinyl leukotriene receptor 1 (CysLT1R) antagonist montelukast suppresses matrix metalloproteinase-13 expression induced by lipopolysaccharide

Wei, Jinsong; Chen, Siyuan; Huang, Chengshuo; Guo, Weixiong; Yang, Shukai; Feng, Bailin; Chu, Jiaqi

doi:10.1016/j.intimp.2017.11.020

Cited by 9 publications

(5 citation statements)

References 19 publications

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“…Of particular further interest are the recent reports that the leukotriene receptor antagonist montelukast not only suppresses inflammation in a poly I:C‐induced asthma exacerbation model in mice, but also suppresses LPS‐induced MMP‐13 expression in mouse osteoblasts . However, the effects of montelukast on bronchial epithelial repair in our model remain to be investigated.…”

Section: Discussionmentioning

confidence: 97%

Targeting matrix metalloproteinase‐13 in bronchial epithelial repair

Howell

Smith

Shute

2018

Clin Experimental Allergy

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Bronchial epithelial repair is limited by endothelin and by MMP-13, a protease that degrades coagulation factors, such as fibrinogen, and matrix proteins essential for epithelial repair. Further studies with primary cells from patients are needed to confirm whether repurposing bosentan and inhibitors of MMP-13 expression or activity, for inhalation may be a useful therapeutic strategy in diseases where repeated cycles of epithelial injury and repair occur, such as asthma and COPD.

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Section: Discussionmentioning

confidence: 97%

Targeting matrix metalloproteinase‐13 in bronchial epithelial repair

Howell

Smith

Shute

2018

Clin Experimental Allergy

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“…In the present study, we have demonstrated that a high RUNX2 expression in MT‐treated rats is correlated to reduced bone loss. RUNX2 is associated with osteoblast differentiation, 38 bone synthesis, and mineralization 39 . Thus, it may be suggested that MT therapeutic effect seems to involve RUNX2 expression and osteoblast activation.…”

Section: Discussionmentioning

confidence: 99%

Leukotriene receptor antagonist reduces inflammation and alveolar bone loss in a rat model of experimental periodontitis

Moro

Oliveira

Santana

et al. 2021

Journal of Periodontology

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Background Leukotrienes (LTs) participate in the process of tissue damage in periodontal disease by leukocyte chemotaxis and osteoclastic activation. The activation of Cysteinyl‐LT receptor is associated with increased expression of proinflammatory molecules and osteoclastogenesis. However, its implications on periodontal disease progression have not been studied. The present study evaluated the effect of the cysteinyl‐LT receptor antagonist (montelukast [MT]) on ligature‐induced experimental periodontitis (EP) in rats. Methods Adult male Wistar rats were subjected to bilateral ligature‐induced periodontitis and orally treated with MT (at doses of 10 or 30 mg/kg/d, MT10, and MT30, respectively). Sham animals had the ligatures immediately removed and received placebo treatment. Sets of animals were euthanized 7, 14, or 21 days after ligature placement and the mandibles were removed for macroscopic evaluation of alveolar bone loss (ABL). In addition, histological analysis of periodontal tissues, myeloperoxidase (MPO) activity of gingival tissues, and periodontal tissue expression of collagen type I, RUNX2, RANK, RANKL, OPG, BLT1, Cys‐LTR1, LTA4H, and LTC4S were also analyzed. Results MT significantly reduced ABL at 14 (MT10 and MT30) and 21 days (MT10) (P < 0.05), gingival MPO at 7 (MT10) and 14 days (MT30) (P < 0.05), LTA4H, BLT1 and LTC4S gene expression on day 14 day (MT30, P < 0.05) and increased RUNX2 expression on day 14 (MT30, P < 0.05). Conclusion Systemic therapy with MT decreases periodontal inflammation and ABL in ligature‐induced periodontitis in rats.

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“…These data suggest that the anti-in ammatory effect of montelukast may account for a decrease in cytokine-related pancreatic injury due to the suppression of the pro-in ammatory mediators. Other studies supported the ability of montelukast to suppress the release of in ammatory markers in LPS-induced injuries to other organs as lung and kidney(Khodir et al, 2014); heart(Khodir et al, 2016); liver(Mohamadin et al, 2011) and LPS-induced bone destruction(Wei et al, 2018). Coskun et al reported that the reduction in pro-in ammatory cytokines (TNF-α and IL-6) when montelukast was administered following the application of cecal ligation and puncture (CLP, a model of polymicrobial sepsis)(Coskun et al, 2011).…”

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confidence: 89%

Inhibition of sepsis-induced pancreatic injury by leukotriene receptor antagonism via modulation of oxidative injury, and downregulation of inflammatory markers in experimental rats

Hagar,

Alhazmi,

Arafah

et al. 2023

Naunyn-Schmiedeberg's Arch Pharmacol

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The purpose of this study is to investigate the effect of montelukast on lipopolysaccharide (LPS)-induced pancreatitis. MethodsAcute pancreatitis was induced by a single dose of LPS (6 mg/kg, i.p.) while montelukast was given in two different doses (10 and 20 mg/kg/day) for three consecutive days prior to injection of LPS. ResultsAcute pancreatitis was demonstrated by signi cant increases in serum levels of pancreatic enzymes lipase and amylase and lactate dehydrogenase (LDH). Proin ammatory response activation was evident by elevated serum levels of nitric oxide (NO) and increased pancreatic concentrations of tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1β) and intercellular adhesion molecule-1 (ICAM-1). The activity of myeloperoxidase (MPO), a neutrophil in ltration marker, has also been increased. Oxidative stress was con rmed by signi cant increases in the concentrations of lipid peroxides measured as thiobarbituric acid reactive substances (TBARS) and decreases in the concentrations of reduced glutathione (GSH) in the pancreatic tissues of animals treated with LPS. Histological examination con rmed the biochemical alterations. Montelukast treatment reversed all these biochemical indices and histopathological changes that were induced by LPS. Montelukast reduced the increase in serum levels of lipase, amylase, LDH, total nitrite/nitrate, TNF-α, IL-1β and ICAM-1. MPO activities and TBARS concentrations were also suppressed while GSH content was increased in pancreatic tissues. ConclusionThese results show that montelukast may be a useful pharmacological agent in protection against LPSinduced oxidative pancreatic injury by inhibiting neutrophil in ltration, counteracting oxidative stress, and suppressing in ammatory mediators.

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The cysteinyl leukotriene receptor 1 (CysLT1R) antagonist montelukast suppresses matrix metalloproteinase-13 expression induced by lipopolysaccharide

Cited by 9 publications

References 19 publications

Targeting matrix metalloproteinase‐13 in bronchial epithelial repair

Targeting matrix metalloproteinase‐13 in bronchial epithelial repair

Leukotriene receptor antagonist reduces inflammation and alveolar bone loss in a rat model of experimental periodontitis

Inhibition of sepsis-induced pancreatic injury by leukotriene receptor antagonism via modulation of oxidative injury, and downregulation of inflammatory markers in experimental rats

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