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공지사항

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  • 2019-02-21 10:58:00
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1.간독성 물질로부터 간 보호작용
2.알코올 분해 작용(알코올 및 아세트알데히드 분해 효소 활성)
3.간세포 단백 합성 증가 및 지방 과산화 억제, 간세포 재생작용

1)Possible role of cytochrome P450 (P450) inhibition by redginseng saponins in carbon tetrachloride (CCl4)-induced lipid peroxidation was investigated in liver microsomes prepared from male Sprague Dawley rats Silymarin revealed more potent protection against CCl4-induced lipid peroxidation Taken together, our present results indicated that the inhibitory effects of red ginseng saponin on P450 enzymes may have a critical role in CCl4-induced lipid peroxidation in ratliver microsomes and that the mechanism of hepatoprotection by red ginseng saponin may be distinct from that of silymarin."
 Sprague Dawley 수컷 쥐의 간 microsomes에서 CCL4로 유도된 지방 과산화에서  홍삼의 cytochrome P450 (P450) 억제 작용 가능한  역할을 연구하였다. Silymarin은 CCL4로 유도된 지방 과산화에 대해 강한 보호 작용을 보였다. 쥐의 간 microsomes에서  CCL4로 유도된 지질 과산화에 중요한 역할을 하는 P450효소에 대한 홍삼사포닌의 억제효과를 보여주며 홍삼 사포닌의 간 보호 작용 기전은  Silymarin과는 현저히 다르다는 것을 보여준다.
2) " Fourteen healthy male volunteers were studied to assess the effects of Panax ginseng on bloodalcohol clearance When the blood alcohol level was compared on individual bases, alcohol concentrations in 10 out of 14 test subjects ranged from 32 to 51% lower than their control values.These results demonstrate that P. ginseng extract enhances blood alcohol clearance in man." 
14명의 건강한 남자 지원자를 대상으로 고려인삼의 혈중 알코올 제거 력 효과를 연구하였다. 알코올 수치를 개인을 기초로 비교 해 볼 때 알코올 농도는 14명 중 10명에서32-52%범위로 대조 치수보다 낮았다. 이결과는 고려인삼이 남자에게서 알코올 제거를 강화하는 것을 보여주는 결과이다. 
3) Hepatitis:"Ginsenoside Ro, an oleanane-type saponinhas been screened for activity in experimental models of acute and chronic hepatitis. Ginsenoside Ro (50 and 200 mg/kg, p.o.) inhibited the increase of serum glutamic oxaloacetic transaminase (s-GOT) and serum glutamic pyruvic transaminase (s-GPT) levels in D-galactosamine (GalN)- and carbon tetrachloride (CCl4)-induced acute hepatitic rats. Ginsenoside Ro inhibited the increase of connective tissue in the liver of CCl4-induced chronic hepatitic rats. Ginsenoside Ro showed a stronger inhibitory effect on the GalN-induced acute hepatitic model than those of the aglycone of ginsenoside Ro, oleanolic acid, or glycyrrhizic acid and its aglycone, glycyrrhetinic acid."
급 만성 간염의 실험적 모델에서 진세노사이드 Ro의 작용을 조사하였다. D-galactosamine (GalN)- and carbon tetrachloride (CCl4)-로 유도된 급성 간염 쥐에서 진세노사이드 Ro는 s-GOT와 s-GPT 수치의 증가를 억제했고 CCL4로 유도된 만성 간염 쥐의 간에서 결합조직의 증가를 억제하였고 GalN로 유도된 급성 간염 모델에서 aglyconeRo이나oleanolic acid , glycyrrhizic acid , aglycone, glycyrrhetinic acid.보다 강력한 억제 효과가 있었다.
4)간 절제를 66% 한 쥐를 대상으로 한 실험에서 Rg1은 MI(mitotic index)을 의미 있게 증가시켰으나 Rb1은 효과가 없었다(Rb1은 경구 투여에 의해 불활성 화 되는 것으로 추측됨))(Cui 1997)
5)간세포의 단백합성 촉진, 간세포 분열촉진, 당과 지방대사 개선, 각종 독성 물질의 해독 촉진작용이 있다.
6)알코올 분해효소 및 아세트 알데하이드 분해효소의 활성을 증진하여 알코올 독성을 경감시킨다.
7)사람을 대상으로 한 실험에서 음주 후 40분 경과 시 혈중 알코올 농도를 40%낮췄다.(0.11%/0.18%)
8)한양 대 의대 구 국희 교수는 B형 바이러스 염 환자를 대상으로 한 임상 실험에서 인삼 투여 시 식욕부진, 소화불량, 두통, 오심, 구토 등의 자각증상의 개선 효과 및 급성 간염의 조기회복 촉진과 만성에 예방에 도움을 준다고 보고하였다.
9)일본 Nissei병원 Yammamoto박사는 만성 감염(C형)에 대한 인삼 투여 시 간 기능의 생화학적 지표 개선에 개선되었으며 소시호 탕 병용 시 개선이 보다 촉진 되었다고 보고하였다.
              문 헌

 

1.Biol Pharm Bull. 2005 Oct;28(10):1992-4

Hepatoprotective effect of 20(S)-ginsenosides Rg3 and its metabolite 20(S)-ginsenoside Rh2 on tert-butyl hydroperoxide-induced liver injury.

? Lee HU, Bae EA, Han MJ, Kim DH. 

College of Pharmacy, Kyung Hee University; Seoul 130-701, Korea.

To evaluate the hepatoprotective effect of Red Ginseng (RG), we isolated a main constituent 20(S)-ginsenoside Rg3 from RG, and its metabolite 20(S)-ginsenoside Rh2 by human intestinal microflora, and investigated their hepatoprotective activities in tert-butyl hydroperoxide (t-BHP)-induced hepatotoxicity of HepG2 cells and mice. When HepG2 cells were treated with t-BHP, its cytotoxicity was significantly increased. 20(S)-Ginsenoside Rh2 potently protected its cytotoxicity, but 20(S)-ginsenoside Rg3 weakly protected it. Intraperitoneally and orally administered 20(S)-ginsenoside Rh2 to t-BHP-injured mice significantly inhibited the increase of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities. Orally administered 20(S)-ginsenoside Rg3 also showed the inhibition against the increase of ALT and AST of t-BHP-induced mice. However, intraperitoneally administered 20(S)-ginsenoside Rg3 could not inhibit the elevation of serum ALT and AST activities. These results suggest that 20(S)-ginsenoside Rg3 a main component of RG may be a prodrug for hepatotoxicity.
PMID: 16204963 [PubMed - indexed for MEDLINE]
20(s)-Rg3와 20(S)-Rh2의 t-BHP로 유도 된 간 손상에 대한 간 보호 효과
홍삼(RG)의 간보호작용을 평가하기위해 Rg3와 장 내 세균에 의한 대사물인 Rh2를 분리하여 tert-butyl hydroperoxide(t-BHP)로 유도된 HepG2과 생쥐의 간독성에 대한 간 보호 작용을 연구하였다. HepG2세포를  t-BHP처리에 의해 세포 독성은 의미 있게 증가하는데 Rh2는 충분히 세포독성을 억제하지만 Rg3는 약하게 방어하였다.IV나 경구로 Rh2를 t-BHP로 유도된 생쥐에 투여하면 혈청 ALT와 AST작용을 증가를 의미있게 억제하였다. 경구로 Rg3를 투여하는 것 역시 ALT와 AST의 억제를 보여주었다. 그러나 IV로 Rg3를 투여하는 것은 ALT나 AST작용을 억제하지 못하였다. 이들 결과는 홍삼의 주요 성분인 Rg3가 간 독성 방어 전구 약물이라 추측 된다

 

 

2.Liver Int. 2005 Oct;25(5):1069-73

Hepatoprotective effect of ginsenoside Rb1 and compound K on tert-butyl hydroperoxide-induced liver injury.

? Lee HU, Bae EA, Han MJ, Kim NJ, Kim DH. 

College of Pharmacy, Kyung Hee University, 1 Hoegi-dong, Dongdaemun-ku, Seoul 130-701, Korea.

BACKGROUND/AIM: The main component of Panax ginseng, which have been reported by many researchers, are ginsenoside Rb1, Rb2 and Rc. Orally administered ginsenosides are metabolized to 20-O-beta-D-glucopyranosyl-20(S)-protopanaxadiol (compound K) by intestinal bacteria and absorbed to blood. To understand its hepatoprotective effect and its mechanism, the effects of ginsenoside Rb1 and its metabolite compound K on chemically injured HepG2 cells and mice were investigated. METHODS: Ginsenoside Rb1 and compound K were isolated from ginseng. Hepatotoxicity of HepG2 cells and mice was induced by tert-butyl hydroperoxide (t-BHP). Cytotoxicity for HepG2 cells and serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) for mice as markers of hepatoprotective activity were measured. RESULTS: Compound K protected HepG2 cell cytotoxicity induced by t-BHP. However, ginsenoside Rb1 did not inhibit cytotoxicity. Nevertheless, both ginsenoside Rb1 and compound K significantly inhibited the increment of ALT and AST induced by t-BHP in mice, when it was orally administered. However, intraperitoneally administered ginsenoside Rb1 did not inhibit the increment of plasma ALT and AST induced by t-BHP in mice. These compounds did not exhibit antioxidant activity. However, compound K showed the potent membrane stabilizing activity more than ginsenoside Rb1. CONCLUSION: Compound K, which was produced from ginsenosides of Panax ginseng in intestine, could protect liver injury.
PMID: 16162168 [PubMed - indexed for MEDLINE]
Rb1과 Compound K의 T-BHP로 유도된 간 손상에서 간 보호효과

배경과 목적:고려인삼의 중요 성분은 Rb1,Rb2,RC 이다 진세노사이드를 경구 투여하면 장내 미생물에 의해 CompoundK로 바뀌어 혈액에 흡수된다. 화학적으로 손상된 HepG2과 생쥐에서 Rb1과 대사물인 Compound K의 간 보호 효과를 이해하기위해 연구를 하였다.
방법:Rb1과 Compound K를 인삼에서 분리하였다. HepG2세포와 생쥐에의 간독성은  t-BHT로 유도되었다. HepG2세포의 세포독성과 와  생쥐의 ALT,AST(간 보호 작용의 표식 자)를 측정하였다.
결과: Compound K는 t-BHT로 유도된 HepG2세포의 세포독성을 보호하였으나 Rb1은 보호하지 못하였다.그럼에도 불구하고 Rb1과 Compound K는   경구 투여 시 t-BHT로 유도된 생쥐에서 의미 있게 ALT와 AST의 증가를 억제하였다. 그러나 Rb1을  복강 내로 투여 시 Rb1은 ALT,AST의 증가를 억제하지 못하였다. 이들 물질은 항 산화 작용을 보이지는 않았으나 Compound K는 Rb1에 비해 충분한 세포막 안정화 작용을 보였다.
결론: 고려인삼의 장내 생성물인  Compound K는 간 손상을 보호한다.

3.Biol Pharm Bull. 2002 Apr;25(4):457-60.
Possible role of ginsenoside Rb1 on regulation of rat liver triglycerides. Park KH, Shin HJ, Song YB, Hyun HC, Cho HJ, Ham HS, Yoo YB, Ko YC, Jun WT, Park HJ.Department of Biomedical Pharmacology, Korea Ginseng and Tobacco Research Institute, Taejon.We have studied the effects of ginsenoside Rb1 (GRb1) on the change in lipid contents in rat liver. When GRb1was administered intraperitoneally to rats, liver microsomal cytochrome P-450 content and NADPH-cytochrome P-450 reductase activity were lower than those in control rats. The contents of triglyceride (TG) and cholesterol were decreased, but those of totalphospholipid, phosphatidylcholine, and phosphatidylethanolamine were increased in the GRb1-treated group compared with controls. These results indicate that GRb1 might be involved in lipid metabolism by regulating the activity of microsomal cytochrome P-450 monooxygenase. Although liver TG levels were reduced by GRb1, the levels of TG and beta-lipoprotein in serum from the GRb1-treated group did not change as compared with those in controls. Thus we suggest that the decrease in liver TG levels with GRb1-treatment is not associated with the secretion of TG-rich very low-density lipoprotein. Furthermore, the level of cAMP was also significantly increased in the GRb1-treated group as compared with that in controls. Additionally, the cAMP level was more markedly increased as compared with that in the GRb1-treated group or control group when GRb, was exogenously added to the reaction system for measuring cAMP production in homogenates from control group liver. Accordingly, these results demonstrate that GRb1 might lower TG levels via cAMP-production in the liver, and GRb1 might be an interesting candidate to for a modulator of cAMP-mediated effects, especially within the liver steatosis system.PMID: 11995924 [PubMed - indexed for MEDLINE]
4. Zhongguo Zhong Xi Yi Jie He Za Zhi. 2000 Sep;20(9):673-6.
[Effect of ginsenosides on proliferation and differentiation of human CD34+ hematopoietic stem/progenitor cells]
Jin J, Tao H, Gao R.Affiliated Hospital of Zhejiang College of TCM, Hangzhou (310006).
OBJECTIVE: To investigate the effect of ginsenosides (GS) on proliferation and differentiation of human CD34+ stem/progenitor cells. METHODS: CD34+ hematopoietic progenitor cells were isolated from umbilical cord blood by using the immune beads sorting system. The cells were exposed to GS of different concentrations in both liquid culture and semi-solid culture, and the elevation rate on proliferation of CD34+ stem/progenitor cells and colony formation were estimated. The cells were marked withmonoclonal antibody and the marker was examined by flow cytometry after incubated with GS for 14 days. RESULTS: GS (5-50 micrograms/ml) could raise the colony production rate of BFU-E, CFU-E, CFU-GM, CFU-GEMM by (87.6 +/- 2.6)%, (63.3 +/- 2.8)%, (58.0 +/-3.1)% and (96.3 +/- 5.5)% respectively (all P < 0.01), and the best effect in improving cell proliferation of CD34+ cells in vitro was obtained when the concentration of GS was 25 micrograms/ml. After incubation with GS for 14 days, number of CD33+ cells was increased by GS in a dose-dependent manner with a peak increasing rate at 200 micrograms/ml. In the presence of GS 50 micrograms/ml, CD15+ cells were reaching the peak. Number of CD71+ and G-A+ cells increased only when the concentration of GS was 25 micrograms/ml. CONCLUSION: GS could not only promote the proliferation but also induce the differentiation of CD34+ hematopoietic stem/progenitor cells, GS may play the role by cooperating with hematopoietic growth factor, and by its growth factor-like function in the regulation of hematopoiesis.
PMID: 11789172 [PubMed - indexed for MEDLINE] 


2.Liver Int. 2005 Oct;25(5):1069-73

Hepatoprotective effect of ginsenoside Rb1 and compound K on tert-butyl hydroperoxide-induced liver injury.

? Lee HU, Bae EA, Han MJ, Kim NJ, Kim DH. 

College of Pharmacy, Kyung Hee University, 1 Hoegi-dong, Dongdaemun-ku, Seoul 130-701, Korea.

BACKGROUND/AIM: The main component of Panax ginseng, which have been reported by many researchers, are ginsenoside Rb1, Rb2 and Rc. Orally administered ginsenosides are metabolized to 20-O-beta-D-glucopyranosyl-20(S)-protopanaxadiol (compound K) by intestinal bacteria and absorbed to blood. To understand its hepatoprotective effect and its mechanism, the effects of ginsenoside Rb1 and its metabolite compound K on chemically injured HepG2 cells and mice were investigated. METHODS: Ginsenoside Rb1 and compound K were isolated from ginseng. Hepatotoxicity of HepG2 cells and mice was induced by tert-butyl hydroperoxide (t-BHP). Cytotoxicity for HepG2 cells and serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) for mice as markers of hepatoprotective activity were measured. RESULTS: Compound K protected HepG2 cell cytotoxicity induced by t-BHP. However, ginsenoside Rb1 did not inhibit cytotoxicity. Nevertheless, both ginsenoside Rb1 and compound K significantly inhibited the increment of ALT and AST induced by t-BHP in mice, when it was orally administered. However, intraperitoneally administered ginsenoside Rb1 did not inhibit the increment of plasma ALT and AST induced by t-BHP in mice. These compounds did not exhibit antioxidant activity. However, compound K showed the potent membrane stabilizing activity more than ginsenoside Rb1. CONCLUSION: Compound K, which was produced from ginsenosides of Panax ginseng in intestine, could protect liver injury.
PMID: 16162168 [PubMed - indexed for MEDLINE]
Rb1과 Compound K의 T-BHP로 유도된 간 손상에서 간 보호효과

배경과 목적:고려인삼의 중요 성분은 Rb1,Rb2,RC 이다 진세노사이드를 경구 투여하면 장내 미생물에 의해 CompoundK로 바뀌어 혈액에 흡수된다. 화학적으로 손상된 HepG2과 생쥐에서 Rb1과 대사물인 Compound K의 간 보호 효과를 이해하기위해 연구를 하였다.
방법:Rb1과 Compound K를 인삼에서 분리하였다. HepG2세포와 생쥐에의 간독성은  t-BHT로 유도되었다. HepG2세포의 세포독성과 와  생쥐의 ALT,AST(간 보호 작용의 표식 자)를 측정하였다.
결과: Compound K는 t-BHT로 유도된 HepG2세포의 세포독성을 보호하였으나 Rb1은 보호하지 못하였다.그럼에도 불구하고 Rb1과 Compound K는   경구 투여 시 t-BHT로 유도된 생쥐에서 의미 있게 ALT와 AST의 증가를 억제하였다. 그러나 Rb1을  복강 내로 투여 시 Rb1은 ALT,AST의 증가를 억제하지 못하였다. 이들 물질은 항 산화 작용을 보이지는 않았으나 Compound K는 Rb1에 비해 충분한 세포막 안정화 작용을 보였다.
결론: 고려인삼의 장내 생성물인  Compound K는 간 손상을 보호한다.

3.Biol Pharm Bull. 2002 Apr;25(4):457-60.
Possible role of ginsenoside Rb1 on regulation of rat liver triglycerides. Park KH, Shin HJ, Song YB, Hyun HC, Cho HJ, Ham HS, Yoo YB, Ko YC, Jun WT, Park HJ.Department of Biomedical Pharmacology, Korea Ginseng and Tobacco Research Institute, Taejon.We have studied the effects of ginsenoside Rb1 (GRb1) on the change in lipid contents in rat liver. When GRb1was administered intraperitoneally to rats, liver microsomal cytochrome P-450 content and NADPH-cytochrome P-450 reductase activity were lower than those in control rats. The contents of triglyceride (TG) and cholesterol were decreased, but those of totalphospholipid, phosphatidylcholine, and phosphatidylethanolamine were increased in the GRb1-treated group compared with controls. These results indicate that GRb1 might be involved in lipid metabolism by regulating the activity of microsomal cytochrome P-450 monooxygenase. Although liver TG levels were reduced by GRb1, the levels of TG and beta-lipoprotein in serum from the GRb1-treated group did not change as compared with those in controls. Thus we suggest that the decrease in liver TG levels with GRb1-treatment is not associated with the secretion of TG-rich very low-density lipoprotein. Furthermore, the level of cAMP was also significantly increased in the GRb1-treated group as compared with that in controls. Additionally, the cAMP level was more markedly increased as compared with that in the GRb1-treated group or control group when GRb, was exogenously added to the reaction system for measuring cAMP production in homogenates from control group liver. Accordingly, these results demonstrate that GRb1 might lower TG levels via cAMP-production in the liver, and GRb1 might be an interesting candidate to for a modulator of cAMP-mediated effects, especially within the liver steatosis system.PMID: 11995924 [PubMed - indexed for MEDLINE]
4. Zhongguo Zhong Xi Yi Jie He Za Zhi. 2000 Sep;20(9):673-6.
[Effect of ginsenosides on proliferation and differentiation of human CD34+ hematopoietic stem/progenitor cells]
Jin J, Tao H, Gao R.Affiliated Hospital of Zhejiang College of TCM, Hangzhou (310006).
OBJECTIVE: To investigate the effect of ginsenosides (GS) on proliferation and differentiation of human CD34+ stem/progenitor cells. METHODS: CD34+ hematopoietic progenitor cells were isolated from umbilical cord blood by using the immune beads sorting system. The cells were exposed to GS of different concentrations in both liquid culture and semi-solid culture, and the elevation rate on proliferation of CD34+ stem/progenitor cells and colony formation were estimated. The cells were marked withmonoclonal antibody and the marker was examined by flow cytometry after incubated with GS for 14 days. RESULTS: GS (5-50 micrograms/ml) could raise the colony production rate of BFU-E, CFU-E, CFU-GM, CFU-GEMM by (87.6 +/- 2.6)%, (63.3 +/- 2.8)%, (58.0 +/-3.1)% and (96.3 +/- 5.5)% respectively (all P < 0.01), and the best effect in improving cell proliferation of CD34+ cells in vitro was obtained when the concentration of GS was 25 micrograms/ml. After incubation with GS for 14 days, number of CD33+ cells was increased by GS in a dose-dependent manner with a peak increasing rate at 200 micrograms/ml. In the presence of GS 50 micrograms/ml, CD15+ cells were reaching the peak. Number of CD71+ and G-A+ cells increased only when the concentration of GS was 25 micrograms/ml. CONCLUSION: GS could not only promote the proliferation but also induce the differentiation of CD34+ hematopoietic stem/progenitor cells, GS may play the role by cooperating with hematopoietic growth factor, and by its growth factor-like function in the regulation of hematopoiesis.
PMID: 11789172 [PubMed - indexed for MEDLINE] 

 

2.Liver Int. 2005 Oct;25(5):1069-73

Hepatoprotective effect of ginsenoside Rb1 and compound K on tert-butyl hydroperoxide-induced liver injury.

? Lee HU, Bae EA, Han MJ, Kim NJ, Kim DH. 

College of Pharmacy, Kyung Hee University, 1 Hoegi-dong, Dongdaemun-ku, Seoul 130-701, Korea.

BACKGROUND/AIM: The main component of Panax ginseng, which have been reported by many researchers, are ginsenoside Rb1, Rb2 and Rc. Orally administered ginsenosides are metabolized to 20-O-beta-D-glucopyranosyl-20(S)-protopanaxadiol (compound K) by intestinal bacteria and absorbed to blood. To understand its hepatoprotective effect and its mechanism, the effects of ginsenoside Rb1 and its metabolite compound K on chemically injured HepG2 cells and mice were investigated. METHODS: Ginsenoside Rb1 and compound K were isolated from ginseng. Hepatotoxicity of HepG2 cells and mice was induced by tert-butyl hydroperoxide (t-BHP). Cytotoxicity for HepG2 cells and serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) for mice as markers of hepatoprotective activity were measured. RESULTS: Compound K protected HepG2 cell cytotoxicity induced by t-BHP. However, ginsenoside Rb1 did not inhibit cytotoxicity. Nevertheless, both ginsenoside Rb1 and compound K significantly inhibited the increment of ALT and AST induced by t-BHP in mice, when it was orally administered. However, intraperitoneally administered ginsenoside Rb1 did not inhibit the increment of plasma ALT and AST induced by t-BHP in mice. These compounds did not exhibit antioxidant activity. However, compound K showed the potent membrane stabilizing activity more than ginsenoside Rb1. CONCLUSION: Compound K, which was produced from ginsenosides of Panax ginseng in intestine, could protect liver injury.
PMID: 16162168 [PubMed - indexed for MEDLINE]
Rb1과 Compound K의 T-BHP로 유도된 간 손상에서 간 보호효과

배경과 목적:고려인삼의 중요 성분은 Rb1,Rb2,RC 이다 진세노사이드를 경구 투여하면 장내 미생물에 의해 CompoundK로 바뀌어 혈액에 흡수된다. 화학적으로 손상된 HepG2과 생쥐에서 Rb1과 대사물인 Compound K의 간 보호 효과를 이해하기위해 연구를 하였다.
방법:Rb1과 Compound K를 인삼에서 분리하였다. HepG2세포와 생쥐에의 간독성은  t-BHT로 유도되었다. HepG2세포의 세포독성과 와  생쥐의 ALT,AST(간 보호 작용의 표식 자)를 측정하였다.
결과: Compound K는 t-BHT로 유도된 HepG2세포의 세포독성을 보호하였으나 Rb1은 보호하지 못하였다.그럼에도 불구하고 Rb1과 Compound K는   경구 투여 시 t-BHT로 유도된 생쥐에서 의미 있게 ALT와 AST의 증가를 억제하였다. 그러나 Rb1을  복강 내로 투여 시 Rb1은 ALT,AST의 증가를 억제하지 못하였다. 이들 물질은 항 산화 작용을 보이지는 않았으나 Compound K는 Rb1에 비해 충분한 세포막 안정화 작용을 보였다.
결론: 고려인삼의 장내 생성물인  Compound K는 간 손상을 보호한다.

3.Biol Pharm Bull. 2002 Apr;25(4):457-60.
Possible role of ginsenoside Rb1 on regulation of rat liver triglycerides. Park KH, Shin HJ, Song YB, Hyun HC, Cho HJ, Ham HS, Yoo YB, Ko YC, Jun WT, Park HJ.Department of Biomedical Pharmacology, Korea Ginseng and Tobacco Research Institute, Taejon.We have studied the effects of ginsenoside Rb1 (GRb1) on the change in lipid contents in rat liver. When GRb1was administered intraperitoneally to rats, liver microsomal cytochrome P-450 content and NADPH-cytochrome P-450 reductase activity were lower than those in control rats. The contents of triglyceride (TG) and cholesterol were decreased, but those of totalphospholipid, phosphatidylcholine, and phosphatidylethanolamine were increased in the GRb1-treated group compared with controls. These results indicate that GRb1 might be involved in lipid metabolism by regulating the activity of microsomal cytochrome P-450 monooxygenase. Although liver TG levels were reduced by GRb1, the levels of TG and beta-lipoprotein in serum from the GRb1-treated group did not change as compared with those in controls. Thus we suggest that the decrease in liver TG levels with GRb1-treatment is not associated with the secretion of TG-rich very low-density lipoprotein. Furthermore, the level of cAMP was also significantly increased in the GRb1-treated group as compared with that in controls. Additionally, the cAMP level was more markedly increased as compared with that in the GRb1-treated group or control group when GRb, was exogenously added to the reaction system for measuring cAMP production in homogenates from control group liver. Accordingly, these results demonstrate that GRb1 might lower TG levels via cAMP-production in the liver, and GRb1 might be an interesting candidate to for a modulator of cAMP-mediated effects, especially within the liver steatosis system.PMID: 11995924 [PubMed - indexed for MEDLINE]
4. Zhongguo Zhong Xi Yi Jie He Za Zhi. 2000 Sep;20(9):673-6.
[Effect of ginsenosides on proliferation and differentiation of human CD34+ hematopoietic stem/progenitor cells]
Jin J, Tao H, Gao R.Affiliated Hospital of Zhejiang College of TCM, Hangzhou (310006).
OBJECTIVE: To investigate the effect of ginsenosides (GS) on proliferation and differentiation of human CD34+ stem/progenitor cells. METHODS: CD34+ hematopoietic progenitor cells were isolated from umbilical cord blood by using the immune beads sorting system. The cells were exposed to GS of different concentrations in both liquid culture and semi-solid culture, and the elevation rate on proliferation of CD34+ stem/progenitor cells and colony formation were estimated. The cells were marked withmonoclonal antibody and the marker was examined by flow cytometry after incubated with GS for 14 days. RESULTS: GS (5-50 micrograms/ml) could raise the colony production rate of BFU-E, CFU-E, CFU-GM, CFU-GEMM by (87.6 +/- 2.6)%, (63.3 +/- 2.8)%, (58.0 +/-3.1)% and (96.3 +/- 5.5)% respectively (all P < 0.01), and the best effect in improving cell proliferation of CD34+ cells in vitro was obtained when the concentration of GS was 25 micrograms/ml. After incubation with GS for 14 days, number of CD33+ cells was increased by GS in a dose-dependent manner with a peak increasing rate at 200 micrograms/ml. In the presence of GS 50 micrograms/ml, CD15+ cells were reaching the peak. Number of CD71+ and G-A+ cells increased only when the concentration of GS was 25 micrograms/ml. CONCLUSION: GS could not only promote the proliferation but also induce the differentiation of CD34+ hematopoietic stem/progenitor cells, GS may play the role by cooperating with hematopoietic growth factor, and by its growth factor-like function in the regulation of hematopoiesis.
PMID: 11789172 [PubMed - indexed for MEDLINE] 

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