Green Tea Saves the Brain in Stroke

A basic compound found in every cell in the body and in an extract of green tea may prevent brain damage caused from stroke, according to two new studies.

In the first study, researchers at the San Francisco Veterans' Affairs (VA) Medical Center (SFVAMC, CA, USA) subjected rats' brains to ischemia for two hours in a model of stroke. The researchers then administered nicotinamide adenine dinucleotide (NAD+) intranasally immediately after reperfusion (the time when stroke damage actually occurs, since brain cells are suddenly exposed to highly reactive, toxic, and unstable oxygen molecules). The researchers found that NAD+ reduced brain cell death from reperfusion by 70-86% compared with rats not given the treatment. The study was published in the January 1, 2007, issue of Frontiers in Bioscience.

NAD+ plays a number of essential roles in cell metabolism. One role is supporting the activity of the DNA repair enzyme poly (adenosine diphosphate-ribose) polymerase (PARP-1), which normally repairs cell damage from brain infection. In response to reperfusion following ischemia or brain trauma, PARP-1 is overactivated, quickly depleting all available NAD+, and is consequently unable to repair cell damage, leading to brain cell death.

In the second study, by the same team of researchers, green tea extract gallotannin (GT) showed similar results to NAD+, reducing brain cell death significantly when administered intranasally up to three hours after reperfusion. GT has been shown to inhibit the action of the enzyme poly (adenosine diphosphate-ribose) glycohydrolase (PARG) - an enzyme closely related to PARP-1 - and in doing so decrease cell death under ischemia-like conditions. The study also showed that GT provided no protection at all against either PARG or apoptosis inducing factor (AIF) when administered intravenously (IV). The results of the study were reported at the 2006 annual meeting of the American Society for Neurosciences, held in Atlanta (GA, USA) during October 2006.

Our experimental results have suggested that NAD+ can produce greater protective effects than GT against ischemia,” said lead author of both studies Weihei Ying, Ph.D., a research scientist at SFVAMC and an assistant adjunct professor of neurology at the University of California, San Francisco (UCSF, USA). "Plus, NAD+ is a fundamental molecule for cell metabolism, so it is known to have relatively low toxicity.”



Related Links:
San Francisco veterans affairs (VA) Medical Center
University of California, San Francisco