Prevention of MPTP induced Parkinson?s disease through the inhibition of neuronal nitric oxide synthase expression in mice by tea phenolic epigallocatechin 3-gallate.

초록

In animal models of Parkinson?s disease (PD), the toxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is mediated by oxidative stress, especially by nitric oxide (NO). Inhibition of excessive NO production in the brain produces a neuroprotective effect against PD induced by MPTP. Green tea containing high levels of (?)-epigallocatechin 3-gallate (EGCG), which has been known to inhibit inducible NO synthase (NOS), was administered to test whether EGCG attenuates MPTP-induced PD in mice through the reduction in the expression of NOSs. Both tea and the oral administration of EGCG prevented the loss of tyrosine hydroxylase (TH)-positive cells in the substantia nigra and of TH activity in the striatum. These treatments also preserved striatal levels of dopamine and its metabolites, 3,4-dihydroxyphenylacetic acid and homovanillic acid. Both tea and EGCG decreased expressions of nNOS in the substantia nigra. Also tea pus MPTP and EGCG puls MPTP treatments decreased expressions of nNOS at the similar levels of EGCG treatment group. Unexpectedly, the expression of iNOS was not detectable in substantia nigra. Therefore, the preventive effects of tea and EGCG on the MPTP-mediated PD can be explained by the inhibition of nNOS in the substantia nigra.