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Montelukast reduces sepsis-induced lung and renal injury in rats
Ahmed E Khodir1, Hamdy A Ghoneim, Mona Abdel Rahim
1a Department of Pharmacology and Toxicology, Faculty of Pharmacy, Delta University, Mansoura, Egypt.
Abstract:
This study was undertaken to examine the effects of montelukast (MNT) on lung and kidney injury in lipopolysaccharide (LPS) induced systemic inflammatory response. Rats were randomized into 5 groups (n = 8 rats/group): (i) Control; (ii) LPS treated (10 mg/kg body mass, by intraperitoneal (i.p.) injection); (iii) LPS + MNT (10 mg/kg, per oral (p.o.)); (iv) LPS + MNT (20 mg/kg, p.o); (v) LPS + dexamethasone (DEX; 1 mg/kg, i.p.). Twenty-four hours after sepsis was induced, the lung or kidney:body mass ratio and percent survival of rats were determined. Creatinine, blood urea nitrogen (BUN), albumin, total protein, and LDH activity were measured. Lung and kidney samples were taken for histological assessment and for determination of their malondialdehyde (MDA) and glutathione (GSH) contents. The expression of tumour necrosis factor α (TNF-α) in tissue was evaluated immunohistochemically. LPS significantly increased the organ:body mass ratio, serum creatinine, BUN, and LDH, and decreased serum albumin and total protein levels. MDA levels increased in lung and kidney tissues after treatment with LPS, and there was a concomitant reduction in GSH levels. Immunohistochemical staining of lung and kidney specimens from LPS-treated rats revealed high expression levels of TNF-α. MNT suppresses the release of inflammatory and oxidative stress markers. Additionally, MNT effectively preserved tissue morphology as evidenced by histological evaluation. These results demonstrate that MNT could have lung and renoprotective effects against the inflammatory process during endotoxemia. This effect can be attributed to its antioxidant and (or) anti-inflammatory properties.
Insights
Montelukast (MNT) protects against lung and kidney damage caused by lipopolysaccharide (LPS) induced inflammation. MNT reduces inflammatory markers and oxidative stress, preserving organ health.
Area of Science:
- Pharmacology
- Toxicology
- Pathology
Background:
- Systemic inflammatory response, often induced by lipopolysaccharide (LPS), can lead to significant lung and kidney injury.
- Oxidative stress and elevated inflammatory markers are key contributors to LPS-induced organ damage.
Purpose of the Study:
- To investigate the protective effects of montelukast (MNT) against lipopolysaccharide (LPS)-induced lung and kidney injury in a rat model.
- To evaluate the impact of MNT on inflammatory and oxidative stress markers in systemic inflammation.
Main Methods:
- Rats were administered LPS to induce systemic inflammation, followed by treatment with varying doses of montelukast (MNT) or dexamethasone (DEX).
- Organ-to-body mass ratios, survival rates, serum biochemical markers (creatinine, BUN, albumin, total protein, LDH), and tissue oxidative stress markers (MDA, GSH) were assessed.
- Histological examination and immunohistochemical analysis for tumor necrosis factor-alpha (TNF-α) were performed on lung and kidney tissues.
Main Results:
- LPS administration significantly increased organ:body mass ratio, serum creatinine, BUN, LDH, and tissue MDA levels, while decreasing serum albumin, total protein, and tissue GSH levels.
- High expression of TNF-α was observed in lung and kidney tissues of LPS-treated rats.
- Montelukast (MNT) treatment dose-dependently suppressed inflammatory and oxidative stress markers and preserved tissue morphology, demonstrating significant renoprotective and lung-protective effects.
Conclusions:
- Montelukast (MNT) exhibits significant protective effects on lung and kidney tissues against LPS-induced systemic inflammation and endotoxemia.
- The renoprotective and lung-protective mechanisms of MNT are likely mediated through its antioxidant and anti-inflammatory properties.
- MNT represents a potential therapeutic agent for mitigating organ injury during severe inflammatory conditions.
