Guest guest Posted December 2, 2008 Report Share Posted December 2, 2008 Antioxid Redox Signal. 2008 Aug 28. [Epub ahead of print] Green tea epigallocatechin 3-gallate accumulates in mitochondria and displays a selective anti-apoptotic effect against inducers of mitochondrial oxidative stress in neurons. Schroeder EK, Kelsey NA, Doyle J, Breed E, Bouchard RJ, Loucks A, Harbison A, Linseman DA. Veterans Affairs Medical Center, Research Service, Denver, Colorado, United States; emilyschroe@.... Epigallocatechin-3-gallate (EGCG) is a major flavonoid component of green tea that displays anti-apoptotic effects in numerous models of neurotoxicity. Although the intrinsic free radical scavenging activity of EGCG likely contributes to its anti-apoptotic effect, other modes of action have also been suggested. Here, we systematically analyzed the anti-apoptotic action of EGCG in primary cultures of rat cerebellar granule neurons (CGNs). The dose-dependent protective effects of EGCG were determined after co-incubation with eight different stimuli that each induced neuronal apoptosis via distinct mechanisms. Under these conditions, EGCG provided significant neuroprotection only from insults which induce apoptosis by causing mitochondrial oxidative stress. Despite this selective anti-apoptotic effect, EGCG did not significantly alter the endogenous activities or expression of Mn2+-superoxide dismutase, glutathione peroxidase, Nrf2 or Bcl-2. Sub-fractionation of CGNs after incubation with 3H-EGCG revealed that a striking 90-95% of the polyphenol accumulated in the mitochondrial fraction. These data demonstrate that EGCG selectively protects neurons from apoptosis induced by mitochondrial oxidative stress. This effect is likely due to accumulation of EGCG in the mitochondria where it acts locally as a free radical scavenger. These properties of EGCG make it an interesting therapeutic candidate for neurodegenerative diseases involving neuronal apoptosis triggered by mitochondrial oxidative stress. PMID: 18754708 [PubMed - as supplied by publisher] Quote Link to comment Share on other sites More sharing options...
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