Jung Kwan Jang has scientifically demonstrated for the first time how red ginseng improves blood cholesterol levels, identifying its ability to suppress the expression of PCSK9, a key protein that triggers hyperlipidemia.
While previous studies had suggested that red ginseng can reduce lipid levels and lower the risk of hyperlipidemia and cardiovascular disease, the precise molecular mechanism had remained unclear.
Jung Kwan Jang’s Laboratory of Product Development revealed the findings through comprehensive proteomics analysis, cell-based studies, and animal models. The results were published in Scientific Reports.
Hyperlipidemia is characterized by elevated levels of low-density lipoprotein cholesterol (LDL-C), reduced high-density lipoprotein cholesterol (HDL-C), and increased triglycerides, all of which are leading risk factors for atherosclerosis, myocardial infarction, stroke, and coronary artery disease.
LDL-C elevation is closely tied to proprotein convertase subtilisin/kexin type 9 (PCSK9), a liver-derived protein that degrades LDL receptors and prevents the removal of LDL-C from the bloodstream. This mechanism makes PCSK9 a critical therapeutic target in hyperlipidemia and cardiovascular disease.
However, some first-line lipid-lowering agents are known to raise PCSK9 levels and cause muscle-related side effects. Injectable PCSK9 inhibitors are available but face challenges such as high costs and the need for frequent administration.
Jung Kwan Jang’s research demonstrated that red ginseng effectively counteracts this pathway. In laboratory studies, when hepatocytes (HepG2 cells) were treated with a standard lipid-lowering drug, PCSK9 expression rose in proportion to dosage. The addition of red ginseng, however, significantly suppressed this rise.
The effect was replicated in animal models. In an acute hyperlipidemia mouse model, oral administration of red ginseng (200 mg/kg for seven days) led to a 57 percent reduction in triglycerides, a 30 percent reduction in total cholesterol, and a 35 percent reduction in LDL-C compared with the control group. HDL-C levels, by contrast, increased by 16 percent, while PCSK9 secretion returned to normal.
Similarly, in a chronic hyperlipidemia rat model induced by an eight-week high-fat diet, red ginseng supplementation reduced triglycerides by 70 percent, total cholesterol by 35 percent, and LDL-C by 65 percent. PCSK9 secretion was also significantly suppressed, restoring lipid levels to near-normal ranges.
“This study confirmed the potential of red ginseng as a preventive and adjunct therapy for hyperlipidemia, given its lipid-improving activity, safety, and convenience of consumption,” said Kim Sang-kyu, research director of Jung Kwan Jang’s Laboratory of Product Development. “We will continue to conduct in-depth research to build stronger scientific evidence for the health benefits of red ginseng.”
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