Green Tea Research Today is a free monthly online journal that collates and summarizes the latest research about Green Tea, including details on benefits, antioxidants, weight loss, diet, side effects. | ||||||||
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Epigallocatechin gallate inhibits nitric oxide-induced apoptosis in rat PC12 cells.Jung JY, Han CR, Jeong YJ, Kim HJ, Lim HS, Lee KH, Park HO, Oh WM, Kim SH, Kim WJ Dental Science Research Institute, School of Dentistry, 2nd Stage of Brain Korea 21 for School of Dentistry, Chonnam National University, Gwangju 500-757, South Korea. Nitric oxide (NO) is associated with many pathophysiology of the central nervous system including brain ischemia, neurodegeneration and inflammation. Epigallocatechin gallate (EGCG) is a major compound of green tea polyphenol that has shown the protective activity against neuronal diseases. This study examined the effect of EGCG on NO-induced cell death in PC12 cells. The administration of sodium nitroprusside (SNP), a NO donor, decreased the cell viability and induced apoptosis showing characterization such as cell shrinkage and chromatin condensation as well as subG1 fraction of cell cycles. EGCG inhibited the cytotoxicity and apoptotic morphogenic changes induced by SNP. EGCG attenuated the production of reactive oxygen species (ROS) by SNP, and ameliorated the SNP-induced Bax to Bcl-2 expression ratio leading to apoptosis. In addition, EGCG prevented the release of cytochrome c from the mitochondria into the cytosol as well as the upregulation of the voltage-dependent anion channel (VDAC), a cytochrome c releasing channel, in the mitochondria of SNP-treated cells. EGCG abrogated the activation of caspase-9, caspase-8 and caspase-3 induced by SNP. These results demonstrate that EGCG has a protective effect against SNP-induced apoptosis in PC12 cells by scavenging ROS and modulating the signal molecules associated with cytochrome c, caspases, VDAC and the Bcl-2 family. These findings suggest that EGCG might be a natural neuroprotective substance. Published 5 December 2006 in Neurosci Lett, 411(3): 222-7.
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