4.5 Article

Baicalein Attenuates Astroglial Activation in the 1-Methyl-4-Phenyl-1,2,3, 4-Tetrahydropyridine-Induced Parkinson's Disease Model by Downregulating the Activations of Nuclear Factor-kappa B, ERK, and JNK

Journal

JOURNAL OF NEUROSCIENCE RESEARCH
Volume 92, Issue 1, Pages 130-139

Publisher

WILEY
DOI: 10.1002/jnr.23307

Keywords

neuroinflammation; Parkinson's disease; NF-B; ERK; JNK

Categories

Funding

  1. Korean National Research Foundation (NRF)
  2. Korea government (MEST) [20090083538]
  3. Research Center for Anti-Aging Technology Development
  4. Ministry of Trade, Industry and Energy [N0000697]

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In Parkinson's disease (PD), neuroinflammation plays a critical role in the neurodegenerative process. Furthermore, activated microglia and astrocytes, responsible for activated immune response in the central nervous system, are found in regions associated with dopaminergic neuronal death. The flavonoid baicalein is known to have antibacterial, antiviral, and antiinflammatory activities. In the present study, the neuroprotective effects of baicalein were examined in a murine 1-methyl-4-phenyl-1,2,3,4-tetrahydropyridine (MPTP) model of PD. Low doses of baicalein improved motor ability and prevented dopaminergic neuron loss caused by MPTP. In addition, microglial and astrocyte activations were reduced in PD mice pretreated with baicalein. Further study of primary astrocytes revealed that baicalein suppressed the 1-methyl-4-phenylpyridine-induced nuclear translocation of nuclear factor-B and reduced the activations of JNK and ERK, suggesting that the neuroprotective effects of baicalein in our PD model were due to attenuated astrocyte activation. The findings of this study indicate that baicalein could be useful for the treatment of PD and other neuroinflammation-related neurodegenerative diseases. (c) 2013 Wiley Periodicals, Inc.

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