Effects of Ginsenosides on Several Signaling Pathways

Ginsenosides is a class of steroidal glycosides derived from the plant genus Panax ginseng, whose biological effects have been evaluated in cell culture or animal models. Animal studies have shown their beneficial therapeutic effects on pathological conditions in different tissues. The ameliorative effects of ginsenosides in different pathogenic conditions can be attributed to their effects on the production of reactive oxygen species. These substances mainly affect the activity of multiple signaling pathways.

For example, in diabetic complications, ginsenosides affect the activity of the PI3K/AKT, GSK-3β, and AMPK pathways, thereby reducing oxidative stress, inflammation, gluconeogenesis, glucose production, lipid accumulation, and insulin resistance (see figure 1) ^[1].

Fig. 1 Effects of ginsenosides on PI3K/AKT, GSK-3β, and AMPK pathways

There are three types of AKT substrates, GSK-3β, FOXO1 and PGC-1α that may be involved in liver glucose production. The activated PI3K/AKT pathway can be involved in insulin metabolism and improved glucose uptake by transporting glucose transporter proteins to the cell membrane and/or facilitating glycogen synthesis by phosphorylation of glycogen synthase kinase 3 (GSK-3β). On the one hand, FOXO regulates insulin responsiveness and glucose homeostasis. In addition, AMPK reduces fat and cholesterol synthesis. Additionally, ginsenosides can inhibit ROS production by activating Nrf-2, HO-1 and AKT. They can also inhibit the NF-кB signaling pathway, which reduces inflammation by blocking mRNA expression of pro-inflammatory mediators and cytokines, including TNF-α, IL-1β, iNOS, and COX-2.

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