Ginsenoside compound K protects human umbilical vein endothelial cells against oxidized low-density lipoprotein-induced injury via inhibition of the NF-κB and p38, JNK MAPK pathways

Oxidized low-density lipoprotein (ox-LDL) caused vascular endothelial cell inflammatory response and apoptosis, acts as an important role in the development and progression of atherosclerosis (AS). Ginsenoside compound K (CK), a metabolite produced by hydrolysis of the ginsenoside Rb1, owns strong anti-inflammatory effects. However, whether CK protects ox-LDL-damaged endothelial cell and the potential mechanisms has not be elucidated.

Systems-level Mechanisms of Action of : A Network Pharmacological Approach

Panax ginseng has long been used since ancient times based on Traditional Asian Medicine theory and clinical experiences, and currently, is one of the most popular herbs in the world. To date, most of the studies with P. ginseng have focused on specific mechanism of actions of individual constituents. However, in spite of many studies on the molecular mechanisms of P. ginseng, it still remains unclear how multiple active ingredients of P. ginseng interact with multiple targets simultaneously, giving the multidimensional effects on various conditions and diseases.

Biosynthesis of rare 20()-protopanaxadiol/protopanaxatriol type ginsenosides through engineered with UDP-glycosyltransferase genes

Ginsenosides are known as the principal pharmacological active constituents in Panax medicinal plants such as Asian ginseng, American ginseng and Notoginseng. Some of the ginsenosides, especially the 20(R) isomers, are trace in natural source and difficult to be chemically synthesized. The present study provides an approach to produce such trace ginsenosides applying biotransformation through E.coli modified with relevent genes.