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    Home > Biochemistry News > Biotechnology News > Sequoia interpretation: maintaining NAD-plus levels can reduce brain damage caused by acute isoemia.

    Sequoia interpretation: maintaining NAD-plus levels can reduce brain damage caused by acute isoemia.

    • Last Update: 2020-09-16
    • Source: Internet
    • Author: User
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    Title Translation: The role of NAD plus in regulating mitochondrial freeblin production in acute brain injury (literature authors) Nina Klimova, Adam Fearnow, Tibor Kristian Published by Brain Sciences (Published) 2020.07 (Impact Factors) 3.332 (Literature Interpretation) Mitochondrials are important organs that determine cell survival and death, and any mitochondrial dysfunction can adversely affect cell survival.
    many diseases are caused by mitochondrial dysfunction and mitochondrial abnormalities.
    , the pathology of the disease can be significantly reduced by improving mitochondrial function.
    increase in mitochondrial freelances is considered to be the main cause of adverse effects on mitochondrial activity in the diseased state.
    , it is generally believed that excessive levels of reactive oxygen are an important factor in cell death in acute brain injury or neurodegenerative diseases.
    physiological conditions, the amount of reactive oxygen produced by mitochondrials depends on the rate at which reactive oxygen is generated and cleared.
    In order to maintain reactive oxygen at normal physiological levels, an antioxidant defense system to remove reactive oxygen exists in the brain mitochondrials, including manganese superoxide dismification enzymes, glutathione, glutathione reductase, glutathione peroxidase, etc.
    is that both the production and removal of reactive oxygen depend on the NADH/NAD-plus ratio.
    , the removal of mitochondrial reactive oxygen is affected by the change of mitochondrial NAD-plus level and its redox state.
    in the case of holistic cerebral isoemia caused by cardiac arrest, oxygen in brain tissue is depleted within seconds, causing brain cells, especially neurons, to trigger the mechanism of excitable toxic cell death.
    restoring oxygen by restoring blood flow is a prerequisite for rescuing brain tissue.
    , but during early isoemia refurbishment, a large amount of reactive oxygen is produced, inducing DNA damage and activating the DNA repair enzyme PARP1.
    the enzyme is based on NAD plus, and the over-activity of PARP1 depletes NAD plus in cells, which in turn depletes cell energy, leading to the death of neurons in the brain.
    studies have shown that supplementing NAD-pregenerative NMN after ishemia damage protects the neurons of the hemass from ishemoth cell death and preserves neuron function.
    role of NAD plus is also reflected in the protein deacetylase SIRTs.
    increase in the degree of acetylation of mitochondrial proteins inhibited its activity.
    ISIL levels were significantly reduced after ISIL injury, and SIRTs activity dependent on NAD plus was inhibited, so mitochondrial protein showed excessive acetylation within the first 24 hours of isoemia injury recovery, reduced manganese hyperoxidase activity, and impaired reactive oxygen removal function.
    the use of NAD-prebiotic NMN therapy can prevent the reduction of mitochondrial NAD-plus after isoemia, inhibiting the increase of reactive oxygen levels.
    all this evidence suggests that by normalizing mitochondrial and cell NAD-plus metabolism, the increase in reactive oxygen during the recovery period after isoemia can be reversed, avoiding impaired nerve function in the brain.
    mitochondrials are the main source of reactive oxygen after acute brain injury or in the development of neurodegenerative diseases.
    mitochondrial antioxidant system caused by NAD-plus depletion in mitochondrials is the main mechanism leading to the large amount of reactive oxygen produced by mitochondrials.
    take NMN to prevent mitochondrial NAD-plus depletion and its negative effects.
    may be a new treatment to improve the prognosis of acute isoemia injury in the brain.
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    (Extended Reading) Reactive oxygen free radicals: including superoxyclytic anion free radicals, hydroxy free radicals, etc., characterized by the containing of a pair of electrons, and therefore will seize the electrons of other substances, so that their own stability.
    oxygen free agents in the body have certain functions, such as immunity and signaling processes.
    but too many reactive oxygen free agents can cause destructive behavior, leading to damage to normal cells and tissues in the body, which can lead to a variety of diseases.
    .
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