• 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.

• Korean Journal of Pharmacognosy
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• v.27 no.4
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• pp.295-300
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• 1996

In a preliminary screening of plant extracts for the antigastritic and antiulcer actions in rats, the extracts of head of Panax ginseng Radix showed positive activity in HCl ethanol-induced gastric lesion. Among the systematic fractions of hexane, chloroform, butanol and water, the most potent butanol fraction reduced significantly HCl ethanol-induced gastric lesion at the oral dose of 500 mg/kg. In pylorus ligated rats, hexane and butanol fraction showed decreases in the volume of gastric secretion and acid output, of which effects were stronger in butanol fraction. Further assays with butanol fraction disclosed that it significantly suppressed the aspirin-induced and Shay ulcer. The butanol fraction at the intraduodenal dose of 500 mg/kg showed significant stimulation of mucus secretion.

• Korean Journal of Pharmacognosy
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• v.33 no.2 s.129
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• pp.151-155
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• 2002

Previously, we have reported that the butanol fraction of the head of Panax ginseng had significant gastroprotective activity on gastritis and gastric ulcer models of rats. Considering the safety of the fraction for development of new anti-ulcerative agent or food supplement, general pharmacological study was carried on. The fraction was revealed that have no influence on spontaneous activity, phenobarbital-induced sleeping time, rotarod test, body temperature, gastro-intestinal motility, respiration and blood pressure. The fraction showed weak analgesic action in writhing syndrome and did not show any sign of acute toxicity in mice.

• Biomolecules & Therapeutics
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• v.15 no.4
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• pp.235-239
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• 2007

In order to evaluate the improvement effects of head of Panax ginseng on chronic arthritis, we have investigated the activity of butanol fraction (BuOH fraction) in vitro and in vivo system. BuOH fraction showed significant inhibition on the elastase activity. Anti-arthritic activity of BuOH fraction was also examined on type II collagen-induced arthritis in DBA/1J mice. Mice were immunized with injection of type II collagen emulsified in Freund's complete adjuvant, followed by a booster injection 21 days later. BuOH fraction(BHPG) was administered at an oral dose of 500mg/kg for 2 weeks from the 1st day boost. The hind paw edema was significantly decreased in the group of treatment with BuOH fraction compared to control. In collagen-induced DBA/1J mice, BuOH fraction did not affected the collagen antibody titer but significantly inhibited the tumor necrosis factoralpha(TNF-${\alpha}$) activity. These results were confirmed with histological evaluation of joint tissues. This study may raise the possibility that the usage of BuOH fraction of head of Panax ginseng as alternative medicine for the relief and prevention of rheumatoid arthritis symptoms.

• Archives of Pharmacal Research
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• v.26 no.11
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• pp.906-911
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• 2003

We previously reported that the butanol (BuOH) fraction of the head of Panax ginseng exhibited gastroprotective activity in peptic and chronic ulcer models. In order to identify the active constituent, an activity-guided isolation of the BuOH faction was conducted with a HCI$.$ethanol-induced gastric lesion model. The BuOH fraction was passed through a silica-gel column using a chloroform-methanol gradient solvent system, and six fractions (frs. 1-6) were obtained. The active fr. 5 was further separated by silica-gel column, to yield 6 subfractions (subfrs. a-f). Subfr. d was composed of ginsenosides Re, Rc and $Rb_1$. The most active constituent was ginsenoside $Rb_1$ ($GRb_1$), a protopanaxadiol glycoside, which was investigated for its anti-ulcer effect. Gastric injury induced by HCI$.$ethanol, indomethacin and pyloric ligation (Shay ulcer) was apparently reduced with oral $GRb_1$ doses of 150 and 300 mg/kg. $GRb_1$ at these dosage significantly increased the amount of mucus secretion in an ethanol-induced model. The anti-ulcer effects were consistent with the result of histological examination. These results suggest that the major active constituent in the head of Panax ginseng is $GRb_1$ and that anti-ulcer effect is produced through an increase in mucus secretion.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.384.3-385
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• 2002

Head of Panax ginseng C. A. Meyer indicates its growth number of years and has been widely used for supplying energy to weaklings or used as vomit. Butanol fraction of Panax ginseng head was significantly effective on gastritis and ulcer models in rats. and also had anti-oxidative properties in the previous study. It has been well established that gastric ulcer is induced by imbalance between aggressive factors and protective factors. and the oxidative reaction makes the lesions on gastric mucosal injury severer. (omitted)

• Biomolecules & Therapeutics
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• v.16 no.3
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• pp.277-285
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• 2008

Panax ginseng C.A. Mayer (Araliaceae, P. ginseng) has been used for the enhancement of vascular and immune functions in Korea and Japan for a long time. Ginsenoside $Rb_1$ and $Rg_3$ isolated from P. ginseng head-part butanolic extract (PGHB) were investigated for anti-inflammatory activity. Ginsenosides and PGHB did not affect the cell viability within $0\;-\;100\;{\mu}g/ml$ concentration to RAW 264.7 murine macrophage cells. Ginsenosides and PGHB inhibited partly lipopolysaccharide (LPS)-induced nitrite production in a dose-dependent manner. The ginsenosides and PGHB showed partially chemical nitric oxide (NO) quenching (maximum 40%) in the cell-free system. Also, ginsenoside $Rb_1$ and $Rg_3$ inhibited markedly approximately 74 and 54% of inducible nitric oxide synthase (iNOS) mRNA transcription from LPS-induced RAW 264.7 cells. Taken together, the inhibitory effect of ginsenosides and PGHB on NO production did not occur as a result of cell viability, but was caused by both the chemical NO quenching and the regulation of iNOS. Additionally, the ginsenoside $Rb_1$ and PGHB inhibited prostaglandin $E_2$ ($PGE_2$) synthesis in a concentration-dependent manner, showed approximately 70-98% inhibition at $100\;{\mu}g/ml$ concentration. And the treatment with ginsenosides and PGHB attenuated partially LPS-upregulated cyclooxygenase-2 (COX-2) gene transcription. Ginsenoside $Rg_3$ suppressed LPS-stimulated interleukin-6 (IL-6) level to the basal in RAW 264.7 cells. From these results, ginsenoside $Rb_1,\;Rg_3$, and PGHB may be useful for the relief and retardation of immunological inflammatory responses and its action may occur through the reduction of inflammatory mediators, including NO, $PGE_2$, and IL-6 production.

• Proceedings of the PSK Conference
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• 2002.04a
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• pp.207.3-208
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• 2002

• Korean Journal of Pharmacognosy
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• v.33 no.3 s.130
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• pp.252-256
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• 2002

In the previous study, we demonstrated that ginsenoside $Rb_1$ isolated from the butanol fraction of the head of Panax ginseng had significant gastroprotective activity on gastritis and gastric ulcer models in rats. It has been well established that drugs to have capacity of scavenging or inhibiting the generation of reactive oxygen radicals prevent the gastric mucosal injury. Ginsenoside $Rb_1$ was tested on HCl ethanol-induced gastritis in rats, DPPH-induced free radical scavenging effect, MDA assay, GSH activity, and SOD activity in gastric tissue. It showed significant inhibition in HCl ethanol-induced gastritis, and al~o significantly increase of GSH activated SOD. We speculate that the protective effect of ginsenoside $Rb_1$ against HCl ethanol-induced gastric mucosal damage is originated from the increase of GSH and the activation of SOD.