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KMID : 0352719930170010001
Journal of Ginseng Research
1993 Volume.17 No. 1 p.1 ~ p.12
Study on The Preventive Effect of Ginsenosides Against Hypercholesterolemia and Its Mechasnism


Abstract
The preventive effect of the saponin fraction of Panax ginseng C.A. Meyer against hypercholesterolemia was demonstrated by assaying the cholesterol and triacylglyceride level of the blood serum and liver of rats fed high-cholesterol diet with
and/or
without ginsenoside. To understand the mechanism of the preventive action of ginsenoside, ginsenoside effect on LDL receptor binding ability, cholesterol level, and cAMP level of Chinese hamster ovary (CHO) Cells cultured under various conditions
were
examined, When LDL (20§¶/ml) was added to the culture medium for CHO cell culture, LDL receptor binding activity of the cell was supressed down to 58% of that of normal group. Ginsenosides at 10E-2% and 10E-3% level (w/v) were shown to exert an
appreciable stimulatory effect on CHO cell LDL receptor activity, which partially overcame the suppression due to the presence of LDL (20§¶/ml) in the medium, Ginsenosides also reduced the increased cholesterol level of test group almost to that
of
normal group, and it increased cAMP level, which was usually reduced to 55% of that of the normal group due to the presence of LDL in the medium. Comparison of Kd and Bmax value of CHO cells cultured under different conditions revealed that this
stimulation was due not to the receptor's binding affinity but to its number. Addition of ginsenoside (10-2%) decreased the uptake of taurocholic acid as much as 20% at the actively transporting everted ileal sacs, but it failed to form a large
mixed
micelles with taurocholic acid, which was one of the proposed mechanisms by which ginsenoside inhibits bile acid reabsorption. From the above results, it seemed likely that ginsenoside prevented hypercholestrolemia by decreasing cholesterol level
in
cells thereby relieving the inhibition of LDL receptor synthesis by cholesterol and also by inhibiting bile acid reabsorption from the small intestine.
KEYWORD
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