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Research 5 |
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| Related Research
-- Studies on Rh1, Rh232 |
More Studies
on Rh1, Rh2 (> 90 articles): |
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Search&db=pubmed&term=Rh*%20ginseng |
Study One |
| Rh2,
a compound extracted from ginseng, hypersensitizes
multidrug-resistant tumor cells to chemotherapy |
| Jia
WW, Bu
X, Philips
D, et al., Can J Physiol Pharmacol.
2004 Jul; 82(7):431-7 |
| Department of Surgery, University
of British Columbia, Vancouver, Canada |
| Rh2 is a ginsenoside extracted
from ginseng that has drawn attention in a
few laboratories in Asian countries because
of its potential tumor-inhibitory effect. In the present study, we tested Rh2 on many
tumor-cell lines for its effects on cell
proliferation, induction of apoptosis, and
potential interaction with conventional chemotherapy
agents. Our results showed that Rh2
inhibited cell growth by G1 arrest at
low concentrations and induced apoptosis at
high concentrations in a variety of tumor-cell
lines, possibly through activation of caspases.
The growth arrest and apoptosis may be mediated
by 2 separate mechanisms. Apoptosis is not
dependent on expression of the wild-type p53
nor the caspase 3. In addition, the apoptosis
induced by Rh2 was mediated through glucocorticoid
receptors. Most interestingly, Rh2 can act
either additively or synergistically with
chemotherapy drugs on cancer cells. Particularly,
it hypersensitized multidrug-resistant breast
cancer cells to paclitaxel. These results
suggest that Rh2 possesses strong tumor-inhibiting
properties, and potentially can be used in
treatments for multidrug-resistant cancers,
especially when it is used in combination
with conventional chemotherapy agents. |
Study Two |
| Ginsenoside
Rh2 induces apoptosis via activation of caspase-1
and -3 and up-regulation of Bax in human neuroblastoma |
| Kim
YS, Jin
SH., Arch
Pharm Res. 2004 Aug;27(8):834-9 |
| In human neuroblastoma
SK-N-BE(2) cells undergoing apoptotic death
induced by ginsenoside Rh2, a dammarane
glycoside that was isolated from Panax ginseng
C. A. Meyer, caspase-1 and caspase-3 were
activated. The expression of Bax was increased
in the cells treated with ginsenoside Rh2,
whereas Bcl-2 expression was not altered.
Treatment with caspase-1 inhibitor, Ac-YVAD-CMK,
or caspase-3 inhibitor, Z-DEVD-FMK, partially
inhibited ginsenoside Rh2-induced cell death
but almost suppressed the cleavage of the
116 kDa PARP into a 85 kDa fragment. When
the levels of p53 were examined in this process,
p53 accumulated rapidly in the cells treated
early with ginsenoside Rh2. These results
suggest that activation of caspase-1 and -3
and the up-regulation of Bax are required
in order for apoptotic death of SK-N-BE(2)
cells to be induced by ginsenoside Rh2,
and p53 plays an important role in the pathways
to promote apoptosis. |
Study Three |
| Inhibitory
effects by oral administration of ginsenoside
Rh2 on the growth of human ovarian cancer
cells in nude mice. |
| Tode
T, Kikuchi
Y, Kita
T, Hirata
J, Imaizumi
E, Nagata
I, J
Cancer Res Clin Oncol. 1993; 120(1-2):24-6 |
| Recently two new compounds,
ginsenosides Rh1 and Rh2, have been isolated
from an ethanol extract of the processed root
of Panax ginseng CA Meyer, and Rh2 (but not
Rh1) has been found to cause growth inhibition
of cultured B16 melanoma cells. We have
also demonstrated that Rh2 caused inhibition
of cultured human ovarian cancer cell (HRA)
proliferation. The effect of oral administration
of Rh2 on tumor growth and survival of nude
mice bearing HRA cells was examined. Nude
mice were inoculated subcutaneously in the
right flank with 10(6) HRA cells. After 7
days of tumor inoculation 2 mg/kg cis-diamminedichloroplatinum(II)
(cisplatin) was administered intraperitoneally
once a week for 5 weeks. In Rh2-treated groups.
Rh2 was dissolved in absolute ethanol, adjusted
with distilled water to 1, 15, and 120 microM,
and 0.4 ml of each concentration was administered
orally by canula every day for 90 days, from
the next day of tumor inoculation. The tumor
volume, hematocrit and body weight were measured
every week. On days 56 and 63 after tumor
inoculation, the tumor volumes in all groups
treated with Rh2 were significantly less than
those in an ethanol-treated control group
and also in cisplatin treated group. After
70 days, the tumor growth in nude mice treated
with 15 microM and 120 microM Rh2 was significantly
inhibited compared to that in a cisplatin
treated group as well as a control group.
Consequently, the survival of nude mice treated
with 15 microM and 120 microM Rh2 was also
significantly prolonged, compared to that
of cisplatin treated mice. No toxic effects
were observed in any of the mice |
Study Four |
| Structure
and biological activity of protopanaxatriol-type
saponins from the roots of Panax notoginseng. |
| Sun
H, Yang
Z, Ye
Y, Int
Immunopharmacol. 2006 Jan;6(1):14-25.
Epub 2005 Jul 26 |
| The further purification
of the total saponins from the roots of Panax
notoginseng by using ordinary and reversed-phase
silica-gel, as well as Sephadex LH-20 chromatography
afford seven adjuvant active protopanaxatriol-type
saponins (PTS), ginsenosides-Rh1 (Rh1),-Rh4
(Rh4),-Rg1 (Rg1),-Re (Re), notoginsenosides-R1
(R1),-R2 (R2),-U (U). These saponins were
evaluated for their haemolytic activities
and adjuvant potentials on the cellular
and humoral immune responses of ICR mice against
ovalbumin (OVA). The effect of the substitution
pattern of these PTS on their biological activities
was investigated and structure-activity relationships
were established. Among seven PTS, the haemolytic
activity of Rh1 was higher than that of other
six compounds (p<0.001) The HD50 values
of Rh4 and U were significantly bigger than
those of R2, Rg1 and Re (p<0.05 or p<0.01).
Seven PTS could significantly increase the
concanavalin A (Con A)-, lipopolysaccharide
(LPS)- and OVA-induced splenocyte proliferation
in the OVA-immunized mice (p<0.01 or p<0.001).
The OVA-specific IgG, IgG1, IgG2a and IgG2b
antibody levels in serum were also significantly
enhanced by seven PTS compared with OVA control
group (p<0.01 or p<0.001). The structure-activity
relationship studies suggested that the number,
the length and the position of sugar side
chains, and the type of glucosyl group in
the structure of PTS could not only affect
their haemolytic activities and adjuvant potentials,
but have significant effects on the nature
of the immune responses. The information
about this structure/function relationship
might be useful for developing semisynthetic
tetracyclic triterpenoid saponin derivatives
with immunological adjuvant activity, as well
as a reference to the distribution of the
functional groups composing the saponin molecule. |
Study Five |
| Molecular
mechanisms of ginsenoside Rh2-mediated G(1)
growth arrest and apoptosis in human lung
adenocarcinoma A549 cells |
| Cheng
CC, Yang
SM, et al., Cancer
Chemother Pharmacol. 2005 Mar 17 |
| Ginsenoside Rh2 (Rh2),
a purified ginseng saponin, has been shown
to have antiproliferative effects in certain
cancer cell types. However, the molecular
mechanisms by which Rh2 affects cell growth
and death have not been fully clarified. In
this study, the antiproliferative effects
of Rh2 in human lung adenocarcinoma A549 cells
were investigated. Treatment of A549 cells
with 30 mug/ml Rh2 resulted in G(1) phase
arrest, followed by progression to apoptosis.
This Rh2-mediated G(1) arrest was accompanied
by the downregulation of the protein levels
and kinase activities of cyclin-D1, cyclin-E
and Cdk6, and the upregulation of pRb2/p130.
In addition, Rh2-induced apoptosis was confirmed
by the TUNEL assay and DNA fragmentation analysis.
Administration of Rh2 caused an increase in
the expression levels of TRAIL-RI (DR4) death
receptor but did not alter the levels of other
death receptors or Bcl-2 family molecules.
Furthermore, the Rh2-induced apoptosis was
significantly inhibited by DR4:Fc fusion protein,
which inhibits TRAIL-DR4-mediated apoptosis.
In addition, caspases-2, -3 and -8 were strongly
activated upon Rh2 treatment. Inhibitors of
caspases-2, -3 and -8 markedly prevented the
cell death induced by Rh2, and inhibitor of
caspase-8 significantly inhibited the activation
of caspases-2, -3 and -8. These observations
indicate that multiple G(1)-related cell cycle
regulatory proteins are regulated by Rh2 and
contribute to Rh2-induced G(1) growth arrest. The increase in the expression levels of DR4
death receptor may play a critical role in
the initiation of Rh2-induced apoptosis, and
the activation of the caspase-8/caspase-3
cascade acts as the executioner of the Rh2-induced
death process. |
More Studies
(> 90 articles): |
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Search&db=pubmed&term=Rh*%20ginseng |
