Powered by PenetrX, with proprietary vectorised green tea catechins and EGCG in a skin-similar phospholipid base.
Green Tea catechins play a role in multiple skin indications. Apart from being a powerful anti-oxidant (approximately 50 times stronger than vitamin C or reseveratrol), they facilitate a number of DNA protection and repair functions.
Note that Green Tea Mask and Green Tea Serum are similar, except that the serum is more than double the concentration of catechins and is in a phospholipid base, designed as a leave-on product, to be layered with other OptoDerm serums and creams.
The high concentration of catechins in Green Tea Mask deliver antioxidant and anti-inflammatory properties to the skin that can help to slow the aging process, maintain the vitality of the skin, and improve its natural tone and glow. Catechins not only decrease skin cell damage directly, by diminishing levels of free radicals, but also inhibit the release of several proteolytic enzymes, especially matrix metalloproteinase enzymes (MMP), that destroy the collagen and elastin in our skin.
- EGCG displays apoptotic, sebosuppressive and anti-inflammatory effects on human sebocytes
- EGCG displays antibacterial effects on the P. acnes bacteria
- EGCG modulates AMPK–SREBP-1 and NF-kB/activator protein 1 (AP-1) signalling pathways, mediating the sebosuppressive and anti-inflammatory effects of EGCG respectively
- EGCG induces cytotoxicity of SEB-1 sebocytes via apoptosis
EGCG improves acne and is well tolerated in a clinical trial setting.
Research has shown that green tea can reduce sun damage. This sun damage reduction is due to its ability to combat free radical damage, not by blocking ultraviolet radiation. It is not a replacement for sunscreen.
it has the ability to repair DNA, protect against free radial damage, and boost the immune system.
Offering potent anti-inflammatory qualities, green tea can help to calm skin disorders such as rosacea and psoriasis.
Cellular senescence means a state of irreversible growth arrest by which normal cells lose the ability to divide generally after about 50 cell divisions. Some cells become senescent after fewer replication cycles as a result of DNA double-strand breaks. This phenomenon, also known as replicative senescence, was first reported by Hayflick and Moorhead observing that normal human fibroblasts were able to enter a state of irreversible growth arrest after serial cultivation in vitro; meanwhile cancer cells did not enter this growth arrest state and proliferated indefinitely. Cellular senescence can be triggered by multiple mechanisms including telomere shortening, the epigenetic depression of the cyclin-dependent kinase (CDK) inhibitor 2A locus, and DNA damage. A study by Chen et al showed that, overall, the condition of the skin of EGCG-treatment groups was improved, the whole structure of skin was better than control groups and the levels of oxidative stress and the expression of relate with EGFR proteins, was significantly higher than control group after EGCG treatment. These findings suggest that EGCG can resist senescence effectively and even reactivate and restore senescent cells.