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Formation of Lipopolysaccharides01:19

Formation of Lipopolysaccharides

1
Lipopolysaccharides (LPS) are crucial components of the outer membrane of Gram-negative bacteria, serving both structural and functional roles. It contributes to membrane stability and protects bacteria from host immune responses. LPS is composed of three major regions—lipid A, a core oligosaccharide, and an O antigen. The biosynthesis and assembly of LPS involve a highly coordinated set of enzymatic reactions and transport mechanisms. Additionally, LPS is recognized as an endotoxin,...
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  6. Melatonin Mediates Cardiac Tissue Damage Under Septic Conditions Induced By Lipopolysaccharide.

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

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View abstract on PubMed

Summary
This summary is machine-generated.

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.
Keywords:
heartinflammationlipopolysaccharidemelatonin

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  • 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.