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Published on: October 17, 2018
Memantine, A NMDA Receptor Inhibitor Attenuate Lipopolysaccharide-Induced Lung Inflammation and Oxidative Damage in
Atlas Gholami1, Mahmoud Hosseini2, Mohammad Hossein Boskabady1,3
1Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Background:
The anti-oxidative and anti-inflammatory effect of memantine (an N-methyl-D-aspartate receptor inhibitor) has been shown. Therefore, the present study aimed to evaluate the preventive effects of memantine against lipopolysaccharide (LPS)-induced sub-acute lung injury in mice.
Methods:
Male C57BL/6 mice (n=30) were randomized in five groups as follows: (1) control (saline containing 10% DMSO); (2) LPS (5 mg/kg, intraperitoneally); and (3, 4, and 5) LPS 5 mg/kg + memantine 5, 10, 20 mg/kg, respectively. Memantine (dissolved in 10% DMSO) was administrated orally three days before the LPS injection and continued for three days after injury induction. Finally, the levels of markers of oxidative stress, malondialdehyde (MDA), catalase (CAT) and superoxide dismutase (SOD), interleukin (IL)-1β, tumor necrosis factor-α (TNF-α), and nitric oxide (NO), were measured and histopathological changes in the lung tissue were assessed.
Results:
Lipopolysaccharide (LPS) administration increased the TNF-α, IL-1β, NO, and MDA, levels, while decreasing the lung tissues activity of CAT (P< 0.05) and SOD (P< 0.001) and caused lung pathological damages. Memantine 20 mg/kg, alleviated LPS-induced injury score, reduced the lung tissue levels of TNF-α, IL-1β, MDA, and NO, and restored CAT activity (P< 0.05, P< 0.01).
Conclusions:
LPS-triggered elevation of lung injury markers including histopathological changes, inflammatory cytokines, and oxidative damage. All pathological changes were suppressed by memantine.
Insights
Memantine, an N-methyl-D-aspartate receptor inhibitor, demonstrated protective effects against lipopolysaccharide-induced lung injury in mice. It reduced oxidative stress and inflammation, mitigating pathological damage.
Area of Science:
- Pharmacology
- Toxicology
- Immunology
Background:
- Memantine exhibits known anti-oxidative and anti-inflammatory properties.
- Lipopolysaccharide (LPS) is a potent inducer of lung injury.
Purpose of the Study:
- To investigate the preventive efficacy of memantine against LPS-induced sub-acute lung injury in a mouse model.
- To assess memantine's impact on oxidative stress and inflammatory markers in lung tissue.
Main Methods:
- Male C57BL/6 mice were divided into five groups: control, LPS-induced injury, and LPS with varying doses of memantine.
- Memantine was administered orally prior to and following LPS injection.
- Levels of oxidative stress markers (MDA, CAT, SOD), inflammatory cytokines (IL-1β, TNF-α), nitric oxide, and lung histopathology were evaluated.
Main Results:
- LPS challenge significantly elevated markers of oxidative stress (MDA, NO) and inflammation (TNF-α, IL-1β), while reducing antioxidant enzyme activity (CAT, SOD) and causing lung damage.
- Memantine treatment, particularly at 20 mg/kg, significantly reduced LPS-induced lung injury scores.
- Memantine administration restored antioxidant enzyme activity and decreased levels of MDA, NO, TNF-α, and IL-1β.
Conclusions:
- Memantine effectively suppressed LPS-induced lung injury in mice.
- The protective effects of memantine are attributed to its ability to mitigate oxidative stress and inflammatory responses.
