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  • 1
    ISSN: 0378-8741
    Language: English
    Titel der Quelle: Journal of ethnopharmacology : an interdisciplinary journal devoted to bioscientific research on indigenous drugs
    Publ. der Quelle: Shannon : Elsevier Science Ireland
    Angaben zur Quelle: Vol. 176 (2015), p. 336-344
    DDC: 610
    Abstract: The modified-Chungsimyeolda-tang (DG) is an important traditional Korean herbal formula used in traditional oriental medicine for treatment of cerebrovascular disorders, including stroke. The formula is based on the book "Dongui Sasang Shinpyun". In the previous studies, the neuroprotective effect of DG is demonstrated in an in vitro Parkinson's disease (PD) model, and in this study, the 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) animal model of PD is used to evaluate the behavioral effect of DG and possible mechanism through anti-apoptosis of DG. 6-Hydroxydopamine (6-OHDA) also is used to evaluate the anti-apoptosis effect of DG in SH-SY5Y cells. MPTP was used to evaluate the behavioral damage and neurotoxicity in mice. The bradykinesia symptom was measured by a Pole test and a Rota-rod test in mice. Also the loss of tyrosine hydroxylase (TH)-positive neurons induced by MPTP was examined by an immunohistochemical assay. The DG-mediated anti-apoptosis effect was measured using an immunoblotting assay with apoptosis-related markers such as Bax and cleaved caspase-3. DG and 1-methyl-4-phenylpyridinium (MPP(+)) were co-treated with primary dopaminergic neurons to evaluate the protective effect of DG. The expression of caspase-3 and PARP was measured to detect the protective effect of DG from the damage by 6-OHDA. The treatment with DG resulted in prophylactic effects on MPTP-induced Parkinsonian bradykinesia and the immunohistochemical analysis showed that DG provided the neuroprotection against the MPP(+)-induced dopaminergic neurons loss through the anti-apoptosis effect. The present results suggested that it might be possible to use DG for the prevention of substantia nigra pars compacta (SNpc) degeneration induced by exposure to the toxic substances, such as MPTP/MPP(+), in PD mouse model.
    Note: Copyright: Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
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  • 2
    ISSN: 0378-8741
    Language: English
    Titel der Quelle: Journal of ethnopharmacology : an interdisciplinary journal devoted to bioscientific research on indigenous drugs
    Publ. der Quelle: Shannon : Elsevier Science Ireland
    Angaben zur Quelle: Vol. 171 (2015), p. 196-204
    DDC: 610
    Abstract: A growing body of literature supports the concept that antiaging herbs may be potential candidates for use in treating age-related neurodegeneration, including Alzheimer׳s disease (AD). Mori Fructus is a well-known traditional herbal medicine, food, and dietary supplement. This study employed models of amyloid beta (Aβ)-induced AD to investigate the protective effects of Mori Fructus ethanol extract (ME) against age-related disease and cognitive deficits. To examine the protective effect of ME, we measured cell viability, cytotoxicity, and survival in rat primary hippocampal cultures. We performed behavioral tests and histological analysis in mouse models of AD induced by Aβ(25-35) toxicity. To investigate the mechanism underlying the protective effect, we performed western blotting using antibodies against apoptotic markers as well as the nonphosphorylated and phosphorylated forms of Akt, glycogen synthase kinase-3β (GSK-3β), and tau. We also measured apoptotic marker fluorescence intensity. ME significantly attenuated Aβ-induced cell damage, enhanced Akt and GSK-3β phosphorylation, and reduced tau phosphorylation. ME reduced apoptotic markers that were activated by GSK-3β, and reduced reactive oxygen species production. Further, ME decreased the B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X expression ratio, mitochondria depolarization, cytochrome c release from mitochondria, and caspase-3 activation. We confirmed that ME treatment improved cognitive impairment and neuronal cell death induced by Aβ(25-35) toxicity in the mouse hippocampus via its antiapoptotic activity. These results indicate that ME protects cognition and neurons in AD-like models induced by Aβ via reduction of tau phosphorylation and apoptosis through GSK-3β inactivation.
    Note: Copyright: Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
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  • 3
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    In:  Journal of ethnopharmacology : an interdisciplinary journal devoted to bioscientific research on indigenous drugs Vol. 134, No. 2 (2011), p. 313-323
    ISSN: 0378-8741
    Language: Undetermined
    Titel der Quelle: Journal of ethnopharmacology : an interdisciplinary journal devoted to bioscientific research on indigenous drugs
    Publ. der Quelle: Shannon : Elsevier Science Ireland
    Angaben zur Quelle: Vol. 134, No. 2 (2011), p. 313-323
    DDC: 610
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
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