• Journal of Ginseng Research
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• v.22 no.1
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• pp.22-31
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• 1998

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-Ht 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 cells isolated from human and rabbit gastric mucosa. Ginseng saponin, ginsenoside $Rb_1$, $Rb_2$, $Rg_1$ and $Rh_2$ 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 concerltration(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 $Rb_1$, $Rb_2$ and $Rh_2$ 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 $Rg_1$ and $Rh_2$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 secretary pathway such as protein phosphorylation or proton pump. Nitric oxide may not be involved in the inhibitory effect of ginseng saponin on stimulated acid secretion.

• Biomolecules & Therapeutics
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• v.4 no.2
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• pp.111-121
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• 1996

Antiulcer effects of Artemisia herba extract (DA-9601) were evaluated in various types of experimental gastric ulcer induced in rats. And the effects of DA-9601 on mucus, basal and stimulated gastric acid secretion were also investigated in rats. DA-9601 (12.5∼400 mg/kg, p.o.) prevented the formation of gastric ulcers induced by 60% EtOH in 150 mM HC1, restraint water immersion stress, platelet activating factor (PAF), aspirin in 150 mM HCI with Pylorus-ligation and indomethacin. DA-9601 (4∼400 mg/kg, p.o.) significantly accelerated the healing rate of acetic acid-induced gastric ulcer and significantly stimulated mucus secretion in a dose-dependent manner. DA-9601 (20∼200 mg/kg, i.d.), however, did not inhibit basal gastric acid secretion in pylorus ligated rats and DA-9601 (200 mg/kg, i.d.) failed to influence histamine-, pentagastrin- and carbachol- stimulated gastric acid secretion. These results suggest that DA-9601 has inhibitory action on gastric lesion and ulceration through increasing mucus secretion in the stomach of rats without influencing basal and stimulated gastric acid secretion.

• Journal of Ginseng Research
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• v.25 no.4
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• pp.141-149
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• 2001

The effect of ginseng on gastric ulcer and gastric acid secretion was investigated in pylorus-ligated rats. Methods: Sprague-Dawley strain rats were used after 24 hours fast. Pylorus-ligation was performed under light ether anaesthesia, then gastric mucosal damage was evoked in conscious pylorus-ligated rats by the administration of subcutaneous (s.c.) indomethancin (20mg/kg), s.c. histamine (150mg/kg) or by pylorus-ligation (Shay ulcer). Ginseng was given by intragastric (i.g.) or intraperitoneal (i.p.) route simultaneously with the ulcerogens. Rats were killed after 3h (indomethacin) and histamine models) or after 18h (Shay ulcer), when the gastric secretory responses, the number and severity of gastric mucosal lesions and mucosal mucus content deetermined. the effect of i.p. ginseng on basal gastric acid secretion and on gastric acide secretion in indomethacin (20mg/kg, s.c.)-treated rats was also investigated in urethane anesthetized rats. Gastric acid secretion was measured by flushing of the gastric lumen with saline every 15min through an oesophageal cannula. Results: In conscious pylorus-ligated rats, i.g. ginseng(12.5-50mg/$m\ell$; 50-200mg/kg) protected against gastric mucosal lesions evoked by s.c. indomethacin or s.c. histanmine in the d3-h pylorus-lighted rat, withoutmodifying gastric acid secretory responses. Ginseng given i.p. (150 or 200mg/kg) did not reduce the gastric lesions produced by histamine or by ligating the pylorus (Shay ulcer) Ginseng given orally in 50mg/$m\ell$ (200mg/kg) increased gastric mucus secretion in saline- and indomethacin-treated conscious pylorus-ligated rats. In anaesthetized rats ginseng (50 or 200mg/kg) did not modify basal gastric acid secretion or gastric acid secretion in the indomethacin-treated rats. Conclusions: ginseng given orally exerts gastroprotective effects in the rat stomach. Such anti-ulcer effect does not involve changes in gastric acid secretory responses. In addition, ginseng possesses stimulatory effect on gastric mucus secretion, which could be one mechanism by which the compound exerts its antiulcer effect. Our data are in favor for a beneficial effect for topically applied ginseng on the gastric mucosa.

• Archives of Pharmacal Research
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• v.12 no.4
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• pp.243-248
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• 1989

Effects of B-HT 920 on the vagally stimulated gastric acid secretion were studied in anesthetized and gastric fistula rats. When the gastric acid secretion was increased by stimulation of the vagus nerve, B-HT 920 was partially attenuated by prazosin, $\alpha_1-$adrenoceptor antagonist and virtually abolished by yohimbine, $\alpha_2-$adrenoceptor antagonist. On the other hand, when the gastric acid secretion was increased by the infusion of bethanechol, a muscarinic parasympathetic stimulant, B-HT 920 had no effect on the bethanechol-induced gastric acid secretion. These results suggest that B-HT 920 inhibits vagally induced gastric acid secretion by activation of presynaptic $\alpha-$adrenoceptors located on the vagally stimulated pathways in the gastric wall and this effect of B-HT 920 is more related to $\alpha_2-$adrenoceptors than $\alpha_1-$adrenoceptors.

• The Korean Journal of Pharmacology
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• v.31 no.1 s.57
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• pp.75-84
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• 1995

Acid secretion and NO synthase activity were determined in isolated gastric glands following hypoxia/reoxygenation and acidosis to investigate the involvement of NO in acid secretion. Isolated gastric glands were exposed to hypoxia (30 min)/reoxygenation (1 h) and/or to acidosis (pH 6.0 and 4.0). Acid secretion was measured by the ratio of $[^{14}C]-aminopyrine$ accumulation between intra- and extraglands. NO synthase activity was determined by percent conversion to $[^{14}C]-citrulline\;from\;[^{14}C]L-arginine$, a precursor of NO. The results indicate that dibutyryl cAMP stimulated acid secretion dose-dependently but had no effect on NO synthase activity in basal gastric glands. Hypoxia/reoxygenation significantly suppressed acid secretion both in unstimulated and stimulated gastric glands, which was exaggerated by acidosis. Constitutive NO synthase, activity, not responded to dibutyryl cAMP, was also inhibited by hypoxia/reoxygenation and acidosis. In conclusion, pathologic state of gastric mucosa such as hypoxia/reoxygenation and acidosis suppresses both acid secretion and NO release but the role of NO in acid secretion stimulated by dibutyryl cAMP in basal gastric glands is not significant.

• The Korean Journal of Pharmacology
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• v.17 no.1 s.28
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• pp.27-32
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• 1981

It has been known that ethanol stimulates the secretion of gastric acid regardless of its route of administration. Recently, however, some studies have challenged this view and claimed that ethanol inhibits the gastric acid secretion. This study was undertaken to investigate the effects of ethanol on the gastric acid secretion in anesthetized rat in respect to the route of administration and the concentration of alcohol. Normal saline (pH adjusted to 6.0) was used as standard perfusion solution and ethanol was mixed as 0.8, 1.7, 5, 10 and 20%. Four ml of perfusion fluid was given into stomach via gastric tube and drained from duodenal tube every 5 min. Acid secretion was measured by back titration to pH 6.0 with N/20 NaOH and expressed as ${\mu}Eq/5$ min. Low concentration of ethanol up to 1.7% in perfusion solution caused little changes in acid secretion, but moderate concentration such as perfusion of 5% or 10% ethanol solution inhibited both the basal and histamine-induced gastric secretion. Moreover, loss of perfused acid was seen by 20% ethanol, which means back diffusion of hydrogen ions into the gastric mucosa. However, intravenous administration of ethanol, maintained at the level of 0.1% alcohol in blood, caused significant stimulation of gastric acid. We, therefore, conclude that in anesthetized rat ethanol has dual effects on acid secretion, i.e., inhibiting and enhancing by oral and intravenous administration, respectively, but further investigation is necessary to clarify these effects.

• YAKHAK HOEJI
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• v.37 no.6
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• pp.581-590
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• 1993

In a preliminary screening of the plant extracts for the antigastritic action in rats, the extract of Aralia elata(Araliaceae) showed positive activity in HCI plus ethanol induced gastric lesion. Systematic fractions with hexane, chloroform, ethyl acetate and butanol resulted in the most patent activity with the butanol fraction: This butanol fraction at the oral dose of 200 mg/kg exhibited significant inhibition of absolute alcohol induced gastric lesion which was more potent than 100 mg/kg of cimetidine and had significant stimulation of mucus secretion. The butanol fraction showed significant decreases in the ulcer indices of Shay ulcers and inhibition of gastric juice secretion with acid output in pylorus-ligated stomachs of rats. It also suppressed the acetic acid induced gastric ulcer. These results might suggest that the butanol fraction had inhibitory action in gastric lesion and ulceration through inhibition of gastric acid secretion and stimulation of mucin secretion in the stomachs of rats.

• Biomolecules & Therapeutics
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• v.3 no.1
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• pp.72-79
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• 1995

The antiulcer effects of newly synthesized prostaglandin derivatives were investigated in various experimental ulcer models and on gastric secretion in rats. HK-3 and HK-4, PG $E_2$derivatives, prevented the formation of acute gastric ulcer induced by ethanol or aspirin in pylorus-ligated rats. The ulcer formation was moderately inhibited by HK-1 and HK-2, PG $F_{2{\alpha}}$ derivatives, and aggravated by SK-1, SK-2 and SK-3, PG $F_{2{\alpha}}$ derivatives. HK-3 and HK-4 reduced the volume, acid output and pepsin output of gastric juice in pylorus-ligated rats. The gastric perfusion with physiologic saline(pH 6.0) showed relatively constant acid secretion and indomethacin increased the acid secretion. The acid secretion was markedly decreased by PG $E_2$but PG $F_{2{\alpha}}$ caused little change. Prostaglandin derivatives, especially HK-3 arid HK-4, significantly inhibited the acid secretion induced by indomethacin. The results show that, PG $E_2$ derivatives, HK-3 and HK-4, inhibit acid secretion and also have protective effects on gastric ulceration induced by ethanol or aspirin.

• Archives of Pharmacal Research
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• v.25 no.1
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• pp.61-66
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• 2002

From our previous result that Panax ginseng head extract had inhibition of gastric damages, the extract was fractionated. Among the hexane, chloroform, butanol and water fractions, butanol fraction Showed the most potent inhibition of HCl.ethanol-induced gastric lesion, aspirin-induced gastric ulcer, acetic acid-induced ulcer and Shay ulcer. Butanol fraction showed significant increase in mucin secretion, and inhibited malondialdehyde (MDA) and $H^{+}/K^{+}ATPase$ activity in the stomach. This results indicate that the effectiveness of the fraction on gastric damages might be related to inhibition of acid secretion, increment of mucin secretion and antioxidant property.

• The Korean Journal of Physiology
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• v.23 no.2
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• pp.393-399
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• 1989

Sixty-seven conscious rats prepared with chronic gastric fistula were studied to examine the effect of vagotomy on gastric secretory responses to medial amygdaloid stimulation. Gastric acid output was significantly increased by electrical stimulation of the medial amygdaloid nucleus, and the increases in acid secretion were completely eliminated by vagotomy. However, in rats subjected to stimulation of the medial amygdaloid nucleus plus vagotomy, acid output was almost same as that in only vagotomized rats. And vagotomy itself decreased the acid secretion significantly. These results indicate that the influence of electrical stimulaton of the medial amygdaloid nucleus on acid secretion is carried largely via vagus nerves. And also, without electrical stimulation of medial amygdaloid nucleus, acid secretion is controlled by way of vagus in rats. Plasma gastrin concentrations were measured following stimulation of the medial amygdaloid nucleus. Plasma levels of gastrin were not significantly altered by stimulation of the medial amygdaloid nucleus with or without vagotomy. It is therefore inferred from the above results that the facilitatory influence of the medial amygdaloid nucleus on the gastric acid secretion is mediated chiefly via vagal activity and that gastrin is not responsible for the increase in acid secretion in this process.