Beneficial effects of natural phenolics on levodopa methylation and oxidative neurodegeneration

Title
Beneficial effects of natural phenolics on levodopa methylation and oxidative neurodegeneration
Authors
강기성Noriko YamabeYujing WenMasayuki FukuiBao Ting Zhu
Keywords
Levodopa; Polyphenol; Methylation; Neurodegeneration; Catechol-O-methyltransferase (COMT); (+)-Catechin; Oxidative neuronal damage; COMT inhibition
Issue Date
2013-02
Publisher
Brain research
Citation
VOL 1497, 1-14
Abstract
Levodopa (L-DOPA) is widely used for symptomatic management in Parkinson's disease. We recently showed that (−)-epigallocatechin-3-gallate, a tea polyphenol, not only inhibits L-DOPA methylation, but also protects against oxidative hippocampal neurodegeneration. In the present study, we sought to determine several other common dietary phenolics, namely, tea catechins [(+)-catechin and (−)-epicatechin] and a representative flavonoid (quercetin), for their ability to modulate L-DOPA methylation and to protect against oxidative hippocampal injury. A combination of in vitro biochemical assays, cell culture-based mechanistic analyses, and in vivo animal models was used. While both tea catechins and quercetin strongly inhibit human liver catechol-O-methyltransferase (COMT)-mediated O-methylation of L-DOPA in vitro, only (+)-catechin exerts a significant inhibition of L-DOPA methylation in both peripheral compartment and striatum in rats. The stronger in vivo effect of (+)-catechin on L-DOPA methylation compared to the other dietary compounds is due to its better bioavailability in vivo. In addition, (+)-catechin strongly reduces glutamate-induced oxidative cytotoxicity in HT22 mouse hippocampal neurons in vitro through inactivation of the nuclear factor-κB signaling pathway. Administration of (+)-catechin also exerts a strong neuroprotective effect in the kainic acid-induced oxidative hippocampal neurodegeneration model in rats. In conclusion, (+)-catechin is a dietary polyphenolic that may have beneficial effects in L-DOPA-based treatment of Parkinson patients by inhibiting L-DOPA methylation plus reducing oxidative neurodegeneration.
URI
http://pubs.kist.re.kr/handle/201004/46164
ISSN
00068993
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