• Proceedings of the Ginseng society Conference
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• 1984.09a
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• pp.13-19
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• 1984

In the previous symposium, authors reported about anti-atherogenic action of Panax ginseng, saying that red-ginseng powder increased serum HDL-cholesterol, decreased total cholesterol, TG, NEFA, in addition, decreased platelet adhesiveness. Later, Toyama group including me. reported that ginsenosides esp. $Rb_2$ enhanced HDL and decreased LDL. Also Matsuyama group and Kinki Univ. group reported that ginsenosides $Rg_1,\;Rb_2,$ etc. inhibited platelet aggregation. This paper will be divided into two parts: Experimental and clinical Experimental study; Using a highcholesterol-cholic acid-fed rats, effects of red ginseng extract and several ginsenosides on serum apoprotein-lipoproteins in relation to prostaglandins. Rats received $2\%$ cholesterol 1-1$\%$ cholic acid diet, ginseng extract or ginsenosides 2.5mg/100g/day for 9 days. Red ginseng extract, ginsenosides $Rb_2,\;Rc,\;Rb_1,\;and\;Rg_1,\;esp.\;Rb_2,$ increased HDL, apo-AI, Aii and $PGI_2,$ while they decreased LDL, apo-B and $TXA_2$. Clinical study: Effect of red ginseng powder on hyperlipidemia was observed. Long term administration of red ginseng powder manufactured by Office of Monopoly, Republic of Korea and offered by Japan-Korea Korean Ginseng Co., Kobe, at the dose of 2.7 g/day, was performed in patients with hyperlipidemia up to 4 years. The significant increase in serum HDL-cholesterol and also the significant decrease in total cholesterol, atherogenic index, TG, NEFA and lipoperoxide was observed with 3-48 month administration of red ginseng. Conclusions: Red ginseng and ginsenosides improved hyperlipidemia in rats and in man, with the improvement of blood apoproteins, lipoproteins and prostaglandins in experimental hyperlipidemic animals.

• 한국유가공학회:학술대회논문집
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• 2007.09a
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• pp.49-58
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• 2007

Inflammatory process leads to the well-known mucosal damage and therefore a further disturbance of the epithelial barrier function, resulting abnormal intestinal wall function, even further accelerating the inflammatory process[1]. Despite of the records, etiology and pathogenesis of IBD remain rather unclear. There are many studies over the past couple of years have led to great advanced in understanding the inflammatory bowel disease(IBD) and their underlying pathophysiologic mechanisms. From the current understanding, it is likely that chronic inflammation in IBD is due to aggressive cellular immune responses including increased serum concentrations of different cytokines. Therefore, targeted molecules can be specifically eliminated in their expression directly on the transcriptional level. Interesting therapeutic trials are expected against adhesion molecules and pro-inflammatory cytokines such as TNF-${\alpha}$. The future development of immune therapies in IBD therefore holds great promises for better treatment modalities of IBD but will also open important new insights into a further understanding of inflammation pathophysiology. Treatment of cytokine inhibitors such as Immunex(Enbrel) and J&J/Centocor(Remicade) which are mouse-derived monoclonal antibodies have been shown in several studies to modulate the symptoms of patients, however, theses TNF inhibitors also have an adverse effect immune-related problems and also are costly and must be administered by injection. Because of the eventual development of unwanted side effects, these two products are used in only a select patient population. The present study was performed to elucidate the ability of TNF-${\alpha}$ antibodies produced in sheep colostrums to neutralize TNF-${\alpha}$ action in a cell-based bioassay and in a small animal model of intestinal inflammation. In vitro study, inhibitory effect of anti-TNF-${\alpha}$ antibody from the sheep was determined by cell bioassay. The antibody from the sheep at 1 in 10,000 dilution was able to completely inhibit TNF-${\alpha}$ activity in the cell bioassay. The antibodies from the same sheep, but different milkings, exhibited some variability in inhibition of TNF-${\alpha}$ activity, but were all greater than the control sample. In vivo study, the degree of inflammation was severe to experiment, despite of the initial pilot trial, main trial 1 was unable to figure out of any effect of antibody to reduce the impact of PAF and LPS. Main rat trial 2 resulted no significant symptoms like characteristic acute diarrhea and weight loss of colitis. This study suggested that colostrums from sheep immunized against TNF-${\alpha}$ significantly inhibited TNF-${\alpha}$ bioactivity in the cell based assay. And the higher than anticipated variability in the two animal models precluded assessment of the ability of antibody to prevent TNF-${\alpha}$ induced intestinal damage in the intact animal. Further study will require to find out an alternative animal model, which is more acceptable to test anti-TNF-${\alpha}$ IgA therapy for reducing the impact of inflammation on gut dysfunction. And subsequent pre-clinical and clinical testing also need generation of more antibody as current supplies are low.