• Journal of Ginseng Research
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• 제22권1호
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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.

• Journal of Ginseng Research
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• 제25권4호
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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.

• Biomolecules & Therapeutics
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• 제4권2호
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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.

• Archives of Pharmacal Research
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• 제12권4호
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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.

• 한국식품영양학회지
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• 제10권3호
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• pp.394-400
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• 1997

Taheebo의 물 추출물 및 methanol 추출물이 위액 분비 및 위염, 위궤양에 미치는 영향에 대하여 검토한 바, 다음가 같은 결과를 얻었다. 1. Shay 기초위액 분비에 대하여 Taheebo methanol 추출물은 위액 분비량 감소, pH의 증가, 산도의 감소를 가져왔다. 2. 염산.aspirin 유발 위염에 대하여 Taheebo 물 추출물 1,000mg/kg의 투여는 위점막 손상을 유의적으로 억제하였다. 3. 염산.ethanol 유발 위염에 대하여 Taheebo 물 추출물과 methanol 추출물 모두 위손상지수가 유의적으로 감소하여, 뚜렷한 억제효과를 보였고, 이는 용량 의존적으로 나타났다. 4. Indomethacin으로 유발시킨 위궤양에 대하여는 Taheebo 물 추출물 1,000mg/kg 투여시에만 유의적인 억제효과를 나타내었다. 5. 구속수침 스트레스 유발 위궤양에 대하여 Taheebo 물 추출물 및 methanol 추출물 모두에게 유의적으로 궤양지수를 감소시켜 탁월한 억제효과를 보였다. 이상의 결과로 볼 때, Taheebo는 흰쥐의 위염 및 위궤양에 유효하다는 것을 인정할 수 있었다.

• Archives of Pharmacal Research
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• 제25권1호
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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.

• 대한약리학회지
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• 제31권1호
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• pp.75-84
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• 1995

NO의 위산분비에 대한 작용을 규명하기 위하여 분리한 토끼위선세포에서 hypoxia/reoxygenation과 acidosis후 위산분비와 NO synthase 활성을 측정하였다. 분리한 위선세포에 30분의 hypoxia와 1시간의 reoxygenation을 주었으며, acidosis를 위하여 배지의 pH를 6.0과 4.0으로 변화시켜 실험하였다. 위산분비는 위선세포 내와 외의 $[^{14}C]-aminopyrine$ 축적비율로 측정하였으며, NO synthase 활성은 NO의 전구물질인 $[^{14}C]L-arginine$으로부터 $[^{14}C]-citrulline$으로의 전환율로 결정하였다. 결과로서 dibutyryl cAMP는 농도 의존적으로 위산분비를 촉진시켰으나 NO synthase 활성엔 영향을 주지 않았다. Hypoxia/reoxygenation은 기초 및 자극 위산분비를 억제하였으며 acidosis에 의해 위산분비억제는 더욱 심화되었다. Constitutive NO synthase 활성 역시 hypoxia/reoxygenation과 acidosis에 의해 억제되었다. 결론적으로 hypoxia/reoxygenation과 acidosis 같은 위점막의 병적상태는 위산분비와 NO 유리를 모두 억제하나, 기초상태의 위선에서 dibutyryl cAMP에 의한 위산분비 촉진에 대한 NO의 직접적인 작용은 확인되지 않았다.

• 약학회지
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• 제37권6호
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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.

• 대한약리학회지
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• 제17권1호
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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.

• Biomolecules & Therapeutics
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• 제3권1호
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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.