Panax ginseng: Inflammation, platelet aggregation, thrombus formation, and atherosclerosis crosstalk

Fig. 1. Schematic diagram of the progression of atherosclerosis. A damaged subendothelium causes the secretion of pro-inflammatory cytokines and the activation of NFκB, allowing free flowing LDL in the periphery to enter the subendothelium where they are modified to oxidized oxLDL. Foam cells form macrophages take up oxLDL. With the release of adhesion factors, peripheral monocytes were attracted to the endothelium where they are able to migrate into the subendothelium. They are capable of differentiating into macrophages, which will also form foam cells. An accumulation of foam cells causes the formation of a necrotic core. Foam cells secrete factors that can causes ECM degradation, causing the formation of a vulnerable plaque. Monocytes can also differentiate into DCs. Other than that, DCs can also migrate into the subendothelium. They secrete factors that recruit T cells that eventually causes VSMC apoptosis and releases metalloproteinases that induces VSMC migration into the intima, forming a fibrous cap. An inflamed subendothelium also secretes factors like vWF, ADP, and collagen, which are agonists for platelet aggregation. With the activation of the coagulation cascade, THR is…

Fig. 2. Panax ginseng and their compounds have been reported to inhibit many factors involved in the progression of atherosclerosis, as summarized in this figure. This shows the potential of Panax ginseng as a therapeutic for atherosclerosis.