Green Tea Extract protects against Stroke
A study suggests the powerful extract of green tea namely EGCG can protect against injury in cerebral infarction a cause of stroke.
Here’s the science abstract and it is heavy. What is saying is that the EGCG can affects biochemistry pathways that cause a cerebral infarction, which is a type of ischemic stroke resulting from a blockage in the blood vessels supplying blood to the brain. It can be atherothrombotic or embolic.
What we don’t know is what dose (the amount of the substance) and the dosage (the frequency of dose and over what timeframe) could have make the significant difference in preventing stroke. However it is another positive report that EGCG can help prevent debilitating health problems. There are many benefits of green tea, but the best way to receive these benefits is to take a quality supplement containing EGCG. The alternative is drinking 20-40 cups of green tea a day!
-Epigallocatechin Gallate Inhibits Asymmetric Dimethylarginine-Induced Injury in Human Brain Microvascular Endothelial Cells
(−)-Epigallocatechin gallate (EGCG) is the main polyphenol component of green tea (leaves of the Camellia sinensis plant). EGCG has been reported to protect human brain microvascular endothelial cells (HBMECs) against injury in several models. However, the exact mechanism is still unclear. In the current study we found that EGCG protected against asymmetric dimethylarginine (ADMA)-induced HBMEC injury, and inhibited ADMA-induced reactive oxygen species production and malondialdehyde expression. At the same time, we found that pretreatment with EGCG attenuated the upregulation of Bax and the downregulation of Bcl-2, thus confirming the cellular protective properties of EGCG against ADMA-induced apoptosis. Furthermore, we found that EGCG inhibited ADMA-induced phosphorylation of ERK1/2 and p-38, whose inhibitors relieved HBMEC injury. In conclusion, EGCG can protect against ADMA-induced HBMEC injury via the ERK1/2 and p38 MAPK pathways, which are involved in the underlying mechanisms of HBMEC injury in cerebral infarction.