인체 및 토끼 위선세포에서 인삼사포닌의 위산분비 매개 신호전달체계에 미치는 영향

Abstract

Antiulcer effects of ginseng saponin, acidic polysaccharide and methanol extract of Panax ginseng in the patients and experimental animals were reported. Postulated action mechanisms of ginseng were histamine-H2 receptor blocking and increasing gastric blood flow. In the present study, the effect of ginsenosides, the biologically active glycosides of ginseng, on gastric acid secretion was examined using gastric knells isolated from human and rabbit gastric mucosa. Ginseng saponin, ginsenoside Rb1, Rb, Rg1 and Rh were tested in unstimulated as well as stimulated gastric cells. Histamine (10-4 M) and 3-isobutyl-1-methylxanthine (10-4 M) were used as secretagogues. To investigate the mechanism of ginsenosides on acid secretion, the levels of cAMP and cGMP were monitored in gastric cells. As a result, high concentration(1mg/ml) of ginseng saponin showed 73∼75% of stimulated acid secretion in control gastric cells. However ginseng saponin had no effect on unstimulated acid secretion and the levels of cGMP and cAMP in gastric cells. Ginsenoside Rb1, Rb and Rh1 significantly inhibited stimulated acid secretion. Gastric cGMP levels were increased by all ginsenosides tested while cAMP levels were increased by all ginsenosides in unstimulated state of gastric cells, but increased by ginsenosides ginsenoside Rg1 and Rh in stimulated state of gastric cells. The results suggest that inhibition of ginseng saponin on gastric acid secretion represents a complex effect of individual ginsenosides, which produce a range of effect on acid secretion. The inhibition site of ginseng saponin on stimulated acid secretion is postulated as post cAMP levels in acid secretory pathway such as protein phosphorylation or prorton pump. Nitric oxide may not be involved in the inhibitory effect of ginseng saponin on stimulated acid secretion.