Botanicals contain bioactive constituents, including some with potential health benefits. Many herbal medicines possess antioxidant properties, which play an important role in therapeutics. Antioxidants are compounds that protect cells against the damaging effects of reactive oxygen species (ROS). When ROS-generating reactions are activated excessively, pathological quantities of ROS are released to create an imbalance between antioxidants and ROS. Oxidative stress has been linked to many different medical conditions, including cancer.
Green tea, which contains powerful antioxidants, is one of the most popular beverages consumed around the world. Of all the antioxidant compounds found in green tea, the major constituents are polyphenols, including phenolic acids and catechins. Catechins from green tea belong to the family of flavonoids that are powerful antioxidants and free iron scavengers. Many botanical flavonoids possess strong antioxidant activities in the cardiovascular system. Effects of green tea on cancer chemoprevention have been attributed to its antioxidant activities. The highest amount off these compounds are found in matcha tea. EGCG is the most abundant and powerful antioxidant in green tea for cancer chemoprevention.
Green tea contains a bioactive called EGCG that makes a natural antioxidant enzyme called GSTP1 that protects your DNA from oxidative stress. By the way, EGCG can also activate tumor suppressor genes that stop cancer cells from growing. – Dr. William li
In studies, EGCG induced cell apoptosis through intrinsic mitochondrial pathway via activation of Caspase-9 in PC3 prostate cancer cells, MCF-7 breast cancer cells and PANC-1, MIA-Pa-Ca-2, Hs 766 T and AsPC-1 pancreatic cancer cells. EGCG has also been shown to induce apoptosis through extrinsic death receptor pathway in MIA-Pa-Ca-2 pancreatic cancer cells via activation of Fas, DR5 and Caspase-8. In addition, EGCG downregulated the expression of anti-apoptotic proteins, such as BCL-2 in PANC-1, MIA-Pa-Ca-2, Hs 766 T and AsPC-1 pancreatic cancer cells, MDA-MB-231 breast cancer cells , NCI-H295 adrenal cancer cells and PC-12 pheochromocytoma cells , BCL-XL in PANC-1, MIA-Pa-Ca-2, Hs 766 T and AsPC-1 cells pancreatic cancer cells and NCI-H295 adrenal cancer cells, survivin in MCF-7 breast cancer cells and NUGC-3 gastric cancer cells ; and XIAP in NCI-H295 adrenal cancer cells . Also, EGCG was found to upregulate the expression of pro-apoptotic proteins, including Apaf-1 and BAD in NCI-H295 adrenal cancer cells and BAK, BAX, BCL-XS and PUMA in PANC-1, MIA-Pa-Ca-2, Hs 766T and AsPC-1 pancreatic cancer cells . Moreover, EGCG induced apoptosis through both intrinsic and extrinsic pathways, regulatory proteins and endoplasmic reticulum stress via activation of caspase-dependent, caspase-independent, death receptors, downregulation of anti-apoptotic proteins BCL-2, BCL-XL and XIAP and upregulation of pro-apoptotic BAD and BAX in NCI-H295 human adrenal cancer cells.