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Melatonin Mediates Cardiac Tissue Damage under Septic Conditions Induced by Lipopolysaccharide
Milan Lazarević1,2, Miloš Kostić1, Tanja Džopalić1
1Department of Immunology, Medical Faculty of Niš, University of Nis, 18000 Niš, Serbia.
International Journal of Molecular Sciences
|October 26, 2024
Summary
Melatonin (MLT) protects rat heart tissue from lipopolysaccharide (LPS)-induced oxidative stress, inflammation, and apoptosis. MLT treatment significantly reduced damage markers, suggesting its therapeutic potential for cardiovascular diseases.
Area of Science:
- Cardiovascular Science
- Molecular Biology
- Pharmacology
Background:
- Lipopolysaccharide (LPS) triggers oxidative stress, inflammation, and apoptosis in cardiac tissue.
- These pathological processes contribute to significant damage in heart tissues.
Purpose of the Study:
- To investigate the protective effects of melatonin (MLT) against LPS-induced cardiac damage.
- To evaluate MLT's impact on oxidative stress, inflammation, and apoptosis markers in rat hearts.
Main Methods:
- Rats were assigned to control, MLT-treated, LPS-treated, or LPS + MLT-treated groups.
- Assessed oxidative stress (TBARS, AOPPs), inflammation (IL-6, iNOS, NO), and apoptosis (caspase-3, -9, DNase) markers.
Main Results:
- LPS significantly elevated oxidative stress, inflammation, and apoptosis markers compared to controls.
- MLT co-treatment markedly reduced TBARS, AOPPs, caspase-3, and DNase activity.
- MLT also decreased IL-6, iNOS, and NO levels, though not to control levels.
Conclusions:
- Melatonin effectively mitigates LPS-induced oxidative stress, inflammation, and apoptosis in rat cardiac tissue.
- Melatonin demonstrates potential as a therapeutic agent for conditions involving oxidative stress and inflammation.
- Further research is needed to explore clinical applications in cardiovascular diseases.
