Neuroprotective Actions of Green Tea Polyphenol, (-)-Epigallocatechin-3-Gallate in Models of Parkinson’s Disease: Gene Targets
Biochemical evidence points to central roles for oxidative stress (OS) and inflammation in neuronal death in both idiopathic and animal models of Parkinson’s disease (PD). Reports from our laboratory, as supported by others, point to the presence of ongoing OS and inflammatory processes occurring selectively in the substantia nigra pars compacta (SNPC) of parkinsonian brains and in animal models of PD.1–4 Therefore, drugs that exhibit free radical-scavenging and iron chelating properties, may serve as potential candidates for the treatment of PD.
KeywordsNeuronal Cell Culture Cell Cycle Pathway Parkinsonian Brain EGCG Concentration Nuclear Factor kappaB Activity
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- 3.Jenner P. and Olanow C.W., 1996, Pathological evidence for oxidative stress in Parkinson’s disease and related degenerative disorders. in: Neurodegeneration and neuroprotection in Parkinson’s disease, C.W. Olanow, P. Jenner, M.B.H. Youdim, eds., Academic Press, London, pp. 24–45.Google Scholar
- 9.Pan M.H., Lin-Shiau S.Y., Ho C.T., Lin J.H., Lin J.K., 2000, Suppression oflypopolysaccharide-induced nuclear factor kappaB activity by theaflavin-3, 3, -digallate from tea and otherpolyphenols through down- regulation of IkappaB kinase activity in macrophages. Biochem. Pharmacol. 59:357–367.PubMedCrossRefGoogle Scholar
- 11.Levites Y., Youdim M.B.H., Maor G. and Mandel, S., 2001a, Attenuation of 6-hydroxydopamine (6-OHDA)-induced nuclear factor-kappaB (NF-kB) activation and cell death by tea extracts in neuronal cultures. Biochem Pharmacol. In press.Google Scholar