Related Experiment Video
Updated: Apr 3, 2026
Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation
Published on: July 6, 2019
Pretreatment with magnesium ameliorates lipopolysaccharide-induced liver injury in mice
Dalia M El-Tanbouly1, Rania M Abdelsalam1, Amina S Attia1
1Pharmacology & Toxicology Department, Faculty of Pharmacy, Cairo University, Cairo, Egypt.
Background:
Lipopolysaccharide (LPS), a component of the outer membrane of Gram-negative bacteria, is involved in the pathogenesis of sepsis. LPS administration induces systemic inflammation that mimics many of the initial clinical features of sepsis and has deleterious effects on several organs including the liver and eventually leading to septic shock and death. The present study aimed to investigate the protective effect of magnesium (Mg), a well known cofactor in many enzymatic reactions and a critical component of the antioxidant system, on hepatic damage associated with LPS-induced endotoxima in mice.
Methods:
Mg (20 and 40mg/kg, po) was administered for 7 consecutive days. Systemic inflammation was induced 1h after the last dose of Mg by a single dose of LPS (2mg/kg, ip) and 3h thereafter plasma was separated, animals were sacrificed and their livers were isolated.
Results:
LPS-treated mice suffered from hepatic dysfunction revealed by histological observation, elevation in plasma transaminases activities, C-reactive protein content and caspase-3, a critical marker of apoptosis. Liver inflammation was evident by elevation in liver cytokines contents (TNF-α and IL-10) and MPO activity. Additionally, oxidative stress was manifested by increased liver lipoperoxidation, glutathione depletion, elevated total nitrate/nitrite (NOx) content and glutathione peroxidase (GPx) activity. Pretreatment with Mg largely mitigated these alternations.
Conclusion:
Pretreatment with Mg protects the liver from the acute injury which occurs shortly after septicemia.
Insights
Magnesium (Mg) pretreatment protects the liver from acute injury caused by lipopolysaccharide (LPS)-induced endotoxemia in mice. This study demonstrates Mg’s protective role against liver damage, inflammation, and oxidative stress during sepsis.
Area of Science:
- Biomedical research
- Toxicology
- Pharmacology
Background:
- Lipopolysaccharide (LPS) from Gram-negative bacteria triggers sepsis pathogenesis.
- LPS induces systemic inflammation and hepatic damage, mimicking sepsis symptoms.
- Magnesium (Mg) is crucial for enzymatic functions and antioxidant defense.
Purpose of the Study:
- To investigate the protective effects of magnesium (Mg) against liver damage in LPS-induced endotoxemia.
- To evaluate Mg's impact on inflammation and oxidative stress markers in a mouse model.
Main Methods:
- Mice received daily oral doses of Mg (20 and 40mg/kg) for seven days.
- LPS (2mg/kg) was administered to induce systemic inflammation.
- Liver and plasma samples were analyzed for damage, inflammation, and oxidative stress markers.
Main Results:
- LPS induced significant hepatic dysfunction, inflammation (elevated cytokines, MPO), and oxidative stress (lipoperoxidation, altered glutathione levels).
- Markers of apoptosis (caspase-3) and liver injury (transaminases) were elevated in LPS-treated mice.
- Mg pretreatment significantly mitigated LPS-induced hepatic damage, inflammation, and oxidative stress.
Conclusions:
- Magnesium (Mg) pretreatment confers significant protection to the liver against acute injury induced by LPS.
- Mg demonstrates therapeutic potential in mitigating liver damage associated with endotoxemia and sepsis.
