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  1. Article: Neuroimmunomodulatory and Neuroprotective Effects of the Flavonoid Apigenin in

    Dourado, Naiara Silva / Souza, Cleide Dos Santos / de Almeida, Monique Marylin Alves / Bispo da Silva, Alessandra / Dos Santos, Balbino Lino / Silva, Victor Diogenes Amaral / De Assis, Adriano Martimbianco / da Silva, Jussemara Souza / Souza, Diogo Onofre / Costa, Maria de Fatima Dias / Butt, Arthur Morgan / Costa, Silvia Lima

    Frontiers in aging neuroscience

    2020  Volume 12, Page(s) 119

    Abstract: Neurodegenerative disorders (ND) are characterized by the progressive and irreversible loss of neurons. Alzheimer's Disease (AD) is the most incident age-related ND, in which the presence of a chronic inflammatory compound seems to be related to its ... ...

    Abstract Neurodegenerative disorders (ND) are characterized by the progressive and irreversible loss of neurons. Alzheimer's Disease (AD) is the most incident age-related ND, in which the presence of a chronic inflammatory compound seems to be related to its pathogenesis. Different stimuli in the central nervous system (CNS) can induce activation, proliferation, and changes in phenotype and glial function, which can be modulated by anti-inflammatory agents. Apigenin (4,5,7-trihydroxyflavone) is a flavonoid found in abundance in many fruits and vegetables, that has shown important effects upon controlling the inflammatory response. This study evaluated the neuroprotective and neuroimmunomodulatory potential of apigenin using
    Language English
    Publishing date 2020-05-15
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2558898-9
    ISSN 1663-4365
    ISSN 1663-4365
    DOI 10.3389/fnagi.2020.00119
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Guanosine Neuroprotection of Presynaptic Mitochondrial Calcium Homeostasis in a Mouse Study with Amyloid-β Oligomers.

    da Silva, Jussemara Souza / Nonose, Yasmine / Rohden, Francieli / Lukasewicz Ferreira, Pâmela C / Fontella, Fernanda Urruth / Rocha, Andréia / Brochier, Andressa Wigner / Apel, Rodrigo Vieira / de Lima, Thais Martins / Seminotti, Bianca / Amaral, Alexandre Umpierrez / Galina, Antonio / Souza, Diogo O

    Molecular neurobiology

    2020  Volume 57, Issue 11, Page(s) 4790–4809

    Abstract: Amyloid-β oligomers (AβOs) toxicity causes mitochondrial dysfunction, leading to synaptic failure in Alzheimer's disease (AD). Considering presynaptic high energy demand and tight ... ...

    Abstract Amyloid-β oligomers (AβOs) toxicity causes mitochondrial dysfunction, leading to synaptic failure in Alzheimer's disease (AD). Considering presynaptic high energy demand and tight Ca
    MeSH term(s) Amyloid beta-Peptides/administration & dosage ; Amyloid beta-Peptides/toxicity ; Animals ; Calcium/metabolism ; Gene Expression Regulation/drug effects ; Glutamic Acid/metabolism ; Guanosine/administration & dosage ; Guanosine/pharmacology ; Hippocampus/drug effects ; Hippocampus/metabolism ; Homeostasis/drug effects ; Male ; Memory/drug effects ; Mice ; Mitochondria/drug effects ; Mitochondria/metabolism ; Mitochondria/ultrastructure ; Neuroprotection/drug effects ; Oxidative Stress/drug effects ; Presynaptic Terminals/drug effects ; Presynaptic Terminals/metabolism ; Synaptosomes/metabolism ; Synaptosomes/ultrastructure
    Chemical Substances Amyloid beta-Peptides ; Guanosine (12133JR80S) ; Glutamic Acid (3KX376GY7L) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2020-08-13
    Publishing country United States
    Document type Journal Article
    ZDB-ID 645020-9
    ISSN 1559-1182 ; 0893-7648
    ISSN (online) 1559-1182
    ISSN 0893-7648
    DOI 10.1007/s12035-020-02064-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: 1,25-Dihydroxyvitamin D

    Longoni, Aline / Kolling, Janaina / Siebert, Cassiana / Dos Santos, João Paulo / da Silva, Jussemara Souza / Pettenuzzo, Letícia F / Meira-Martins, Leo Anderson / Gonçalves, Carlos-Alberto / de Assis, Adriano M / Wyse, Angela T S

    Nutrition research (New York, N.Y.)

    2017  Volume 38, Page(s) 52–63

    Abstract: Because homocysteine (Hcy) is a risk factor for cardiovascular disease, and vitamin D deficiency can contribute to cardiovascular pathologies. In the present study, we tested the hypothesis that Hcy could impair energy metabolism, mitochondrial function, ...

    Abstract Because homocysteine (Hcy) is a risk factor for cardiovascular disease, and vitamin D deficiency can contribute to cardiovascular pathologies. In the present study, we tested the hypothesis that Hcy could impair energy metabolism, mitochondrial function, and redox status in heart slices of Wistar rats and that 1,25-dihydroxivitamin D
    Language English
    Publishing date 2017-02
    Publishing country United States
    Document type Journal Article
    ZDB-ID 582432-1
    ISSN 1879-0739 ; 0271-5317
    ISSN (online) 1879-0739
    ISSN 0271-5317
    DOI 10.1016/j.nutres.2017.01.007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: 1,25-Dihydroxyvitamin D3 exerts neuroprotective effects in an ex vivo model of mild hyperhomocysteinemia.

    Longoni, Aline / Kolling, Janaina / dos Santos, Tiago M / dos Santos, João Paulo / da Silva, Jussemara Souza / Pettenuzzo, Letícia / Gonçalves, Carlos-Alberto / de Assis, Adriano M / Quincozes-Santos, André / Wyse, Angela T S

    International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience

    2015  Volume 48, Page(s) 71–79

    Abstract: Elevated plasma homocysteine (Hcy) levels have been detected in patients with various neurodegenerative conditions. Studies of brain tissue have revealed that hyperhomocysteinemia may impair energy metabolism, resulting in neuronal damage. In addition, ... ...

    Abstract Elevated plasma homocysteine (Hcy) levels have been detected in patients with various neurodegenerative conditions. Studies of brain tissue have revealed that hyperhomocysteinemia may impair energy metabolism, resulting in neuronal damage. In addition, new evidence has indicated that vitamin D plays crucial roles in brain development, brain metabolism and neuroprotection. The aim of this study was to investigate the neuroprotective effects of 1,25-dihydroxivitamin D3 (calcitriol) in cerebral cortex slices that were incubated with a mild concentration of Hcy. Cerebral cortex slices from adult rats were first pre-treated for 30 min with one of three different concentrations of calcitriol (50 nM, 100 nM and 250 nM), followed by Hcy for 1h to promote cellular dysfunction. Hcy caused changes in bioenergetics parameters (e.g., respiratory chain enzymes) and mitochondrial functions by inducing changes in mitochondrial mass and swelling. Here, we used flow cytometry to analyze neurons that were double-labelled with Propidium Iodide (PI) and found that Hcy induced an increase in NeuN(+)/PI cells but did not affect GFAP(+)/Pi cells. Hcy also induced oxidative stress by increasing reactive oxygen species generation, lipid peroxidation and protein damage and reducing the activity of antioxidant enzymes (e.g., SOD, CAT and GPx). Calcitriol (50 nM) prevented these alterations by increasing the level of the vitamin D receptor. Our findings suggest that using calcitriol may be a therapeutic strategy for treating the cerebral complications caused by Hcy.
    MeSH term(s) Animals ; Antioxidants/metabolism ; Calcitriol/pharmacology ; Cerebral Cortex/drug effects ; Dose-Response Relationship, Drug ; Electron Transport Complex II/metabolism ; Electron Transport Complex IV/metabolism ; Flow Cytometry ; Glial Fibrillary Acidic Protein/metabolism ; Homocysteine/pharmacology ; In Vitro Techniques ; Male ; Neuroprotective Agents/pharmacology ; Phosphopyruvate Hydratase/metabolism ; Propidium/metabolism ; Rats ; Rats, Wistar ; Sodium-Potassium-Exchanging ATPase/metabolism
    Chemical Substances Antioxidants ; Glial Fibrillary Acidic Protein ; Neuroprotective Agents ; Homocysteine (0LVT1QZ0BA) ; Propidium (36015-30-2) ; Electron Transport Complex II (EC 1.3.5.1) ; Electron Transport Complex IV (EC 1.9.3.1) ; Phosphopyruvate Hydratase (EC 4.2.1.11) ; Sodium-Potassium-Exchanging ATPase (EC 7.2.2.13) ; Calcitriol (FXC9231JVH)
    Language English
    Publishing date 2015-12-02
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 605533-3
    ISSN 1873-474X ; 0736-5748
    ISSN (online) 1873-474X
    ISSN 0736-5748
    DOI 10.1016/j.ijdevneu.2015.11.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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