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更新時間：2019-06-28

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產(chǎn)品活性：Rotenone是線粒體電子傳遞鏈復(fù)合物I抑制劑。

研究領(lǐng)域：metabolic Enzyme/Protease

作用靶點：Mitochondrial metabolism

In Vitro: Mitogen Activated Protein Kinase (MAPK), Toll-like receptor, Wnt, and Ras signaling pathways are intensively involved in the effect of rotenone on the ENS. Rotenone-induced cell death is reduced by MCE treatment as measured by decline in the levels of pro-apoptotic proteins. Moreover, MCE treatment significantly augments the levels of anti-apoptotic Bcl2 and blocks the release of cytochrome c, thereby alleviating the rotenone-induced dopaminergic neuronal loss, as evidenced by tyrosine hydroxylase (TH) immunostaining in the striatum.

In Vivo: Rotenone causes a significant increase in the excitatory amino acid neurotransmitters; glutamate and aspartate together with a significant decrease in the inhibitory amino acids, GABA, glycine and taurine are observed in the cerebellum of rat model of PD. Rotenone (1.5, 2, or 2.5 mg/kg) causes a dose-dependent increase in α-synuclein in the substantia nigra. Furthermore, at 2 and 2.5 mg/kg, rotenone causes a significant decrease in the number of tyrosine hydroxylase-immunoreactive neurons in the substantia nigra, and dopamine in the striatum in rats.

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