Submitted to: Nutritional Neuroscience
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: December 23, 2008
Publication Date: June 6, 2009
Citation: Panickar, K.S., Polansky, M.M., Anderson, R.A. 2009. Green tea polyphenols attenuate glial swelling and mitochondrial dysfunction following oxygen-glucose deprivation in cultures. Nutritional Neuroscience. Interpretive Summary: This article describes the protective role of dietary green tea polyphenols in a cell culture model of ischemia/stroke. A major feature of cerebral ischemia is the swelling of cells that result in the development of brain edema. Our results suggest that swelling of glial cells, when deprived of oxygen and glucose, can be significantly prevented by green tea polyphenols. Our results also indicate that the combination of lower concentrations of polyphenols was more effective than any one polyphenol component of green tea extract. One mechanism by which green tea polyphenols exert such protective effects is possibly through protecting the function of mitochondria, an important organelle in the cell that is responsible for energy generation. This information is important to nutritional scientists interested in the basis for the activity of nutrient polyphenols in the regulation of cell function.
Technical Abstract: Astrocyte swelling is a major component of cytotoxic brain edema in ischemia. Oxidative stress and mitochondrial dysfunction have been hypothesized to contribute to such swelling in cultures. We investigated the protective effects of polyphenol-rich green tea extract (GTE) on key features of ischemic injury, namely cell swelling, nitric oxide (NO) production, and depolarization of the inner mitochondrial membrane potential. C6 glial cultures were subjected to 5 hr oxygen-glucose deprivation (OGD) and cell volume was determined using the 3-O-methyl-glucose method. At ninety minutes after the end of OGD, cell volume increased by >33% and this increase was attenuated by GTE, but not by the individual polyphenol components including catechin, epicatechin, or epigallocatechin gallate (EGCG). However, a combination of catechin, epicatechin, and EGCG prevented swelling. OGD-induced increase in NO was further increased by GTE. OGD-induced decline in inner mitochondrial membrane potential was also attenuated by green tea extract, EGCG, and a combination catechin, epicatechin, and EGCG, but not by catechin or epicatechin alone. Our findings indicate a protective effect of GTE in cell swelling in ischemic injury. Such protective effects may be mediated by its effect on the mitochondria. It appears that effects on cell swelling are mediated by the concerted action of more than one of the individual components of GTE.