• Biomolecules & Therapeutics
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• v.7 no.2
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• pp.138-144
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• 1999

Recent studies have suggested that Panax ginseng saponins may stimulate pancreaticobiliary secretion. However, the precise mechanisms underlying the alterations in pancreaticobiliary function associated with ginseng saponins remain uncertain. We studied the effects of ginseng saponins and devazepide, cholecys-tokinin receptor antagonist, on pancreaticobiliary secretion in male Sprague-Dawley rats. The saponins tested were crude saponin (TS) and panaxatriol saponin (PTS). After single or two weeks administration of saponins, pancreaticobiliary juice of rats was collected for 8hrs. Single administration of TS and PTS did not change the volume of pancreaticobiliary juice compared with control group. In contrast, the pretreatment of devazepide significantly increased the volume of pancreaticobiliary juice. The amylase activity was significantly increased by acute TS treatment, but this increase was inhibited by devazepide pretreatment. In animals with two weeks administration of TS and PTS, the volume of pancreaticobiliary juice was not increased as compared to the control group. However, the volume of pancreaticobiliary juice was significantly increased by devazepide treatment. The amylase activity was significantly increased by two weeks administration TS and PTS respectively. This increase was inhibited by devazepide treatment. Our findings suggest that ginseng saponins, especially panaxatriol, increase the amylase activity in pancreaticobiliary juice, and this is, in part, caused by release of endogenous cholecystokinin.

• The Korean Journal of Pharmacology
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• v.17 no.1 s.28
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• pp.17-25
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• 1981

No evidence has accumulated that lead compound is an essential component for biological function in animals. Lead is absorbed primarily through the epithelial mucosal cells in duodenum and the absorption can be enhanced by the substances which bind lead and increase its solubility. Iron, zinc and calcium ions, however, decrease the absorption of lead without affecting its solubility, probably by competing for shared absorptive receptors in the intestinal mucosa. Therefore, the absorption of lead is increased in iron deficient animals. Lead shows a strong affinity for ligands such as phosphate, cysteinyl and histidyl side chains of proteins, pterins and porphyrins. Hence lead can act on various active sites of enzymes, inhibiting the enzymes which has functional sulfhydryl groups. lead inhibits the activity of ${\delta}$-aminolevulinic acid dehydratase for the biosynthesis of hemoproteins and cytochrome, which catalyzed the synthesis of monopyrrole prophobilinogen from ${\delta}$-aminolevulinic acid. Accordingly lead decrease hepatic cytochrome p-450 content, resulting an inhibition of the activity of demethylase and hydroxylase in liver. Little informations are available on the effect of lead on digestive system although the catastrophic effects of lead intoxication are well documented. The present study was, therefore, attempted to investigate the effect of lead on pancreaticobiliary secretion in rats. Albino rats of both sexes weighing $170{\sim}230g$ were used for this study. The animals were divided into one control and three treated groups, i.e., control (physiologic saline 1.5ml/kg i.p.), lead acetate $(l0{\mu}mole/kg/day\;i.p.)$, $Pb(Ac)_2$ and EDTA$(each\;10{\mu}mole/kg/day\;i.p.)$, $Pb(Ac)_2$ and $FeSO_4(each\;l0{\mu}mole/kg/day\;hp)$. The pancreatico-biliary juice was collected under urethane anesthesia, and activities of amylase and lipase were determined by employing Sumner's and Cherry and Crandall's methods. The summarized results are follows. 1) In the experiment for acute toxicity of lead acetate, 20% of mortality was observed in rat treated with lead acetate as well as inhibition of the activity of amylase in the juice at the 3 rd day of the treatment. 2) No increases in body weight were observed in rats treated with lead acetate, while in control group the significant increases were observed. However, the body weights of animals were increased in the group lead acetate plus EDTA or $FeSO_4$. 3) Lead acetate decreased significantly the volume of pancreatico-biliary juice whereas additional treatment of EDTA and $FeSO_4$ prevented it. 4) Total activity of amylase was markedly reduced due to lead acetate treatment, but no change was showed following additional treatment with EDTA and $FeSO_4$. 5) No changes in the cholate and lipase output were observed in rats treated with lead acetate as compared with that of control rats. 6) Increase in bilirubin output in rats treated with lead acetate was shown on the 2nd and 3rd weeks treatment. 7) In the case of in vitro experiment, lead acetate also markedly inhibited release of amylase from pancreatic fragment. 8) Histologic finding indicated that acini vacuolation was induced in the pancreatic tissue of rat treated with lead acete. From the above results, it might be concluded that lead acetate decreases the volume of pancreatico-biliary secretion and inhibits the amylase activity, by acting directly on pancreatic cells.