Stevenleaf
Catalog No: CFN99189
1. Gypenosides (Gyp, Stevenleaf) induce apoptosis in human hepatoma cells through the up-regulation of Bax and Bak, and down-regulation of Bcl-2, release of mitochondrial cytochrome c and activation of caspase cascade.
2. Gypenosides induce ER stress and production of reactive oxygen species and Ca 2+ , change the ratio of Bcl-2 and Bax, followed by the dysfunction of mitochondria, cause cytochrome c release, activation of caspase-3 before leading to apoptosis, these results provide information towards an understanding of the mechanisms by which Gyp induces cell cycle arrest and apoptosis in human tongue cancer cells.
3. Gypenosides can inhibit invasion and migration of human tongue SCC4 cells by down-regulating proteins associated with these processes, resulting in reduced metastasis.
4. Gypenosides imply their remarkable preventative and therapeutic potential in treatment of neurological diseases involving glutamate and oxidative stress.
5. The extensive antioxidant effect of gypenosides may be valuable to the prevention and treatment of various diseases such as atherosclerosis, liver disease and inflammation.
Steviol
Catalog No: CFN93068
Steviol, a natural sweetener, it inhibits proliferation of the gastrointestinal cancer cells intensively. Steviol can treat polycystic kidney disease, it slowed cyst growth, in part, by reducing AQP2 transcription, promoted proteasome, and lysosome-mediated AQP2 degradation. Steviol can induce a significant increase in CYP3A29 expression.
Stevioside
Catalog No: CFN99548
Stevioside is a safe natural sweetener, has no allergic reactions, suited for both diabetics, and PKU patients, as well as for obese persons intending to lose weight by avoiding sugar supplements in the diet. Stevioside enjoys a dual positive effect by acting as an antihyperglycemic and a blood pressure-lowering substance, it may have therapeutic potential in the treatment of type 2 diabetes and the metabolic syndrome.Stevioside exerts anti-inflammatory and anti-apoptotic properties by inhibiting the release of cytokines and the activation of TLR2 and proteins of the NF-κB and MAPK signaling pathways, as well as caspase-3 and Bax.