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  11. Mannan-binding Lectin Inhibits Oxidative Stress-induced Senescence Via The Nad+/sirt1 Pathway

Mannan-binding lectin inhibits oxidative stress-induced senescence via the NAD+/Sirt1 pathway

Yiming Lei1, Jie Meng1, Haiqiang Shi2

  • 1Xinxiang Key Laboratory of Immunoregulation and Molecular Diagnostics, School of Medical Technology, Xinxiang Medical University, Xinxiang 453003, China.

International Immunopharmacology
|June 21, 2024

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View abstract on PubMed

Summary
This summary is machine-generated.

Mannan-binding lectin (MBL) combats oxidative stress and premature aging by activating the NAD+/Sirt1 pathway. This research shows MBL

Area of Science:

  • Biochemistry
  • Cell Biology
  • Immunology

Background:

  • Oxidative stress accelerates cellular and organismal aging.
  • Mannan-binding lectin (MBL) is crucial for innate immunity, anti-inflammation, and anti-oxidation, impacting health and longevity.
  • The role of MBL in mitigating oxidative stress-induced senescence requires further investigation.

Purpose of the Study:

  • To evaluate the role of MBL in oxidative stress-induced premature aging.
  • To explore the underlying molecular mechanisms of MBL's action in aging.
  • To investigate MBL's effects in both a mouse model and cell culture.

Main Methods:

  • Establishment of a D-galactose-induced oxidative premature senescence model in C57BL/6 mice.
  • Utilizing a hydrogen peroxide (H2O2)-induced oxidative senescence model in mouse embryonic fibroblasts (NIH/3T3).
Keywords:
Mannan-binding lectinNicotinamide adenine dinucleotideOxidative stressSenescence

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  • Assessing MBL's impact on senescence markers, oxidative stress, DNA damage, mitochondrial function, and the NAD+/Sirt1 pathway.

    • Main Results:

    • MBL-deficient mice exhibited accelerated aging phenotypes, cognitive deficits, liver damage, and increased senescence markers (p53, p21, SA-β-Gal) and inflammation (IL-1β, IL-6).
    • MBL intervention in NIH/3T3 cells reversed oxidative stress-induced senescence, reducing ROS, DNA damage, and G1 arrest.
    • MBL activated the NAD+/Sirt1 pathway, upregulated NAMPT, and inhibited p38 phosphorylation, counteracting oxidative stress effects.

    Conclusions:

    • MBL effectively inhibits oxidative stress-induced premature aging.
    • MBL's mechanism involves activating the NAD+/Sirt1 pathway.
    • These findings suggest MBL as a potential therapeutic target for delaying oxidative aging.
    Sirtuin 1