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    Home > Active Ingredient News > Study of Nervous System > Cell Death Dis: 菪 improves the survival of dopamine-energy neurons.

    Cell Death Dis: 菪 improves the survival of dopamine-energy neurons.

    • Last Update: 2020-10-05
    • Source: Internet
    • Author: User
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    Parkinson's disease (PD) is a neuro-motor disorder, mainly manifested in abnormal movement caused by the sexual loss of dopamine neurons.
    clinical manifestations include muscle stiffness, slow movement, resting tremors, and posture imbalance.
    Although changes in genetic factors have been shown to be related to the cause of the disease, the exponential accumulation of environmental factors such as reactive oxygen (ROS) triggers a series of circulatory chain reactions, resulting in the accumulation of cellular inclusions, mitochondrial dysfunction and antioxidant loads, which ultimately accelerate the occurrence of the disease.
    the oxidative stress response in PD was further confirmed in the ROS-induced Parkinson's disease model, and elevated oxidation-related markers were also detected in clinical PD samples.
    , regulating the oxidation load of neurons has become one of the main methods of PD therapy.
    researchers have found that Scopoletin , a common derivative of most herbal medicines, is an effective antioxidant with strong neuroresistance.
    Sp can prevent cell oxidation damage by effectively recovering glutathione (GSH), thereby increasing cell resistance to ROS.
    sp-treated cells show higher also prototype glutathione loads and are resistant to interference from oxidants or neurotoxin MPP plus.
    in the PD fruit fly genetic model, Sp can restore redox balance, mitochondrial function and prevent oxidative damage, and ultimately promote the recovery of dopamine neural networks and motor ability.
    researchers found that combined use of Sp could improve the effectiveness of the drug by reducing the chronic toxicity of L-DOPA.
    Sp promotes the recovery of dopamine-energy neurons, the study reveals that Sp can prevent dopamine-energy neuron damage mediated by oxidative stress, while enhancing the efficacy of dopamine supplementation therapy.
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