Ginsenoside Compound K/Ginsenoside CK powder

Ginsenoside Compound k is derived from the dried roots of the Araliaceae plant Panax ginseng C. A. Mey. It is the main metabolite and final absorption form of diol-type ginsenosides in the human intestine.

CK is a non-natural ginsenoside that can be converted from other diol-type ginsenosides. Due to the specificity of the glycosidic bonds at positions 3 and 20 of the tetracyclic triterpene core structure of ginsenoside, CK can only be obtained by mild biotransformation methods, and the commonly used acid or alkali hydrolysis methods are not feasible. At present, bioconversion methods usually include enzymatic conversion and microbial fermentation.

With the continuous breakthrough of the bottleneck of CK preparation, CK, as the functional entity of diol-type ginsenosides, has been studied more and more extensively and deeply on its activity. After nearly ten years of research, people have found that CK has good biological activity in many aspects, and in some aspects even exceeds the existing first-line drugs. The medicinal value of CK has also received more and more attention.

As we age, the skin becomes dry and wrinkles appear, which is closely related to the reduction of hyaluronic acid (HA) in the skin tissue. Using HaCaT cells as a model study, the mechanism of CK in delaying skin aging was studied at the genetic level. It was found that the hyaluronic acid synthase 2 (HAS2) gene changed most significantly after the cells were exposed to CK. After incubation with 1 μmol L-1 CK for 24 h, the HA expression increased from 72.6 ng mL-1 to 238.7 ng mL-1. Nude mouse skin tests have confirmed that CK can significantly increase the HA content in the epidermis and papillary dermis, and significantly increase the thickness of the epidermis. Topical application of CK can delay the occurrence of dryness, wrinkles and other aging phenomena in the skin.

In the experiment of inhibiting the synthesis of prostaglandin E2 and the release of NO in RAW 264.7 cells, the inhibition rate of CK was 2.6 times that of azelastine. However, CK does not inhibit the activity of hyaluronidase, nor does it remove reactive oxygen species, so the anti-allergic effect of CK may be achieved by stabilizing the cell membrane.

Western blotting analysis showed that CK down-regulated the expression of ERK and Art proteins, thereby blocking the activity of NF-κB, while inhibiting the activity of TPA-induced cox-2 gene activator AP-1, ultimately inhibiting the expression of COX-2. And CK can effectively inhibit the production of PGE2 (prostaglandin E2) induced by TPA and restore it to normal levels, thereby achieving the purpose of anti-inflammation and inhibiting tumor proliferation.

In vivo and in vitro tests have shown that CK has a better protective effect on liver damage than the first-line chronic hepatitis treatment drugs silymarin and diphenyl diester, and is a good candidate drug for treating hepatitis and protecting the liver.

Tohda et al. used Abeta(25-35)-induced Alzheimer’s disease (AD) mouse model to study the repair effect of CK on memory damage. The results show that CK can significantly increase the levels of NF-H and synaptophysin in the cerebral cortex and hippocampal circuits, promote axonal extension, reverse axonal neuritis atrophy and synaptic loss, thereby improving memory impairment in AD patients.

Ginsenoside CK is widely used in the fields of medicine, health products and cosmetics

Has anti-inflammatory, anti-aging and other effects