Clinical Trial of a Triterpenoid Liquorice Compound in Gastric and Duodenal Ulcer

Doll, Richard; Hill, Ivor D.; Hutton, Colleen; Underwood, Diana

doi:10.1016/s0140-6736(62)92588-6

Cited by 200 publications

(75 citation statements)

References 14 publications

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“…Growth hormone decreased the num ber of stress erosions and increased the heal ing rate in damaged rat gastric mucosa [13,14). Carbenoxolone also increased the heal ing rate of ulcers in dogs and humans [15,16). These agents were reported to stimulate the DNA synthetic activity of rat gastric mu cosa [ 17,18].…”

Section: Discussionmentioning

confidence: 99%

Effect of Cell Proliferation on Healing of Gastric and Duodenal Ulcers in Rats

Takeuchi¹,

Johnson²

1986

Digestion

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The healing of acetic acid-induced gastric and duodenal ulcers was examined together with the biochemical indices of growth in gastric and duodenal mucosa in the following three groups of rats: (a) chow-fed, (b) fed an isocaloric liquid diet, (c) fed the liquid diet plus pentagastrin injections (250 μg/kg, 3 times/day). Animals received the diet regimen for 10 days from 1 day after induction of ulcer (day 0). Following the feeding regimens, serum gastrin levels, oxyntic gland mucosal DNA synthesis, and gastric secretory function were significantly lowered in the rats fed liquid diets. DNA synthesis in the duodenal mucosa was not different from the pre-ulcer levels. Pentagastrin significantly restored the DNA synthetic and gastric secretory activity of the liquid diet-fed rats toward the levels in the chow-fed group. In the latter group, a significant increase in DNA synthesis and levels of serum gastrin was found at day 6 (after 5 days feeding), which corresponded with a rapid, spontaneous healing of ulcers. Feeding rats liquid diet significantly delayed the healing of gastric, but not duodenal ulcers. Repeated administration of pentagastrin accelerated gastric ulcer healing in the liquid diet group toward the rate observed in the chow-fed group, but had no effect on the healing of duodenal ulcers. These results indicate that cell proliferation is an important factor in the healing of gastric ulcers.

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Section: Discussionmentioning

confidence: 99%

Effect of Cell Proliferation on Healing of Gastric and Duodenal Ulcers in Rats

Takeuchi¹,

Johnson²

1986

Digestion

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“…Glycyrrhizin is an aqueous extract of licorice root. Antiinflammatory, anti-ulcerous and anti-viral effects of glycyrrhizin and glycyrrhizinic acid were reported from 1950s [17][18][19]. Experimental evidence has demonstrated that glycyrrhizin is hepatoprotective in vitro, probably by preventing changes in cell membrane permeability and providing membrane stabilization [20,21].…”

Section: Discussionmentioning

confidence: 99%

Efficacy of Intravenous Glycyrrhizin in the Early Stage of Acute Onset Autoimmune Hepatitis

et al. 2011

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“…Glycyrrhetinic acid (GA) is an aglycone of glycyrrhizin, another major active component of licorice root [1], and is a representative medicine with a long history of use in orien tal pharmacology [2][3][4][5][6], GA has much stronger inhibitory activity than glycyrrhizin in 12-0-tetradecanoylphorbol-13-acetate-induced glucose transport, and has stronger binding acitivity to mineralocorticoid and glucocorticoid receptors [7], GA exists in 18a-and 18P-stereoisomcric forms [8,9], but 18|3-GA is more effective than 18a-GA as an antimuta gen, anti-tumor-initiating agent [9], Previous studies have demonstrated that GA had a re markable inhibitory effect on the antigen-stimulated hista mine release in cultured mast cells (CMCs) [10]. The mech anism of GA action on mast cells has been suggested to be mediated by some effect on phospholipid metabolism, which is generally assumed to be involved in the induction of an antigen-stimulated cellular response in sensitized mast cells [11,12], Some anti-inflammatory steroids antag onize murine skin tumor promotion, and a number of pro tein kinase C (PKC) inhibitors have antitumor activity in vi vo [13][14][15].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Histamine Synthesis by Glycyrrhetinic Acid in Mast Cells Cocultured with Swiss 3T3 Fibroblasts

Lee

Hirota

Jippo-Kanemoto

et al. 1996

Int Arch Allergy Immunol

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The effect of glycyrrhetinic acid (18-O-β-glycyrrhetinic acid, GA) on histamine metabolism was investigated in cultured mast cells (CMCs) cocultured with Swiss 3T3 fibroblasts. GA strongly inhibited histamine synthesis in the cocultured CMCs. Since 50 μM GA inhibited about 80% of histidine decarboxylase (HDC) activity, the inhibitory activity of GA for histamine synthesis was considered to be derived from the inhibition of HDC activity. The number of berberine-sulfate-positive cells also decreased in the presence of GA, which indicated that maturation of CMCs was inhibited by GA. Furthermore, we examined the effect of GA on the mRNA expression of novel protein kinase C δ (nPKCδ), a major isoform of CMCs, by Northern blot analysis. The expression of nPKCδ mRNA in the presence of GA was significantly lower than in the absence of GA. These results suggest the possibility that the inhibition of histamine synthesis by GA is regulated by nPKCδ.

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Clinical Trial of a Triterpenoid Liquorice Compound in Gastric and Duodenal Ulcer

Cited by 200 publications

References 14 publications

Effect of Cell Proliferation on Healing of Gastric and Duodenal Ulcers in Rats

Effect of Cell Proliferation on Healing of Gastric and Duodenal Ulcers in Rats

Efficacy of Intravenous Glycyrrhizin in the Early Stage of Acute Onset Autoimmune Hepatitis

Inhibition of Histamine Synthesis by Glycyrrhetinic Acid in Mast Cells Cocultured with Swiss 3T3 Fibroblasts

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