20(R)-Ginsenoside-Rh19, a novel ginsenoside from alkaline hydrolysates of total saponins in stems-leaves of Panax ginseng / 中草药

Objective: To study the chemical constituents of alkaline hydrolysates of total saponins from the stems and leaves of Panax ginseng. Methods: The chemical constituents were isolated and purified by various chromatographic methods, and the chemical structures were identified by NMR and MS spectra analyses. Results: A total of 30 compounds were isolated and identified. Among them, 28 were determined as 20(S)-protopanaxadiol (1), 20(R)-protopanaxadiol (2), dammar-20(21),24-diene-3β,6α,12β-triol (3), dammar-20(22)E,24-diene-3β,6α,12β-triol (4), 20(S)-protopanaxatriol (5), 20(R)-protopanaxatriol (6), 20(S)-ginsenoside Rh2 (7), 20(R)-ginsenoside Rh2 (8), ginsenoside Rh16 (9), isoginsenoside Rh3 (10), 20(S)-dammar-3β,6α,12β,20,25-pentol (11), 20(R)-dammar-3β,6α,12β,20,25-pentol (12), ginsenoside Rk3 (13), 20(S)-ginsenoside Rh1 (14), 20(R)-ginsenoside Rh1 (15), ginsenoside F1 (16), ginsenoside Rh19 (17), 20(R)-ginsenoside Rh19 (18), dammar-20(22)E-ene-3β,6α,12β,25-tetrol (19), notoginsenoside T2 (20), ginsenoside Rg6 (21), 20(22)E-ginsenoside F4 (22), ginsenoside Rk1 (23), 20(S)-ginsenoside Rg3 (24), 20(R)-ginsenoside Rg3 (25), 20(S)-ginsenoside Rg2 (26), 20(R)-ginsenoside Rg2 (27), and 3β,6α,12β,25-tetrahydroxy-dammar-20(22)E-ene-6-O-α-L-rhamno- pyranosyl-(1→2)-β-D-glucopyranoside (28). Conclusion: Compound 18 is a new saponin. Compounds 3, 4, 11, 12, and 19 are rare dammarane-type triterpenes, and 7-10, 13-18, and 20-28 are rare ginsenosides.

Chemical constituents in acid hydrolysates of total saponins from stems and leaves of Panax ginseng / 中草药

Objective: To study the chemical constituents in the acid hydrolysates of total saponins from the stems and leaves of Panax ginseng. Methods: The chemical constituents were isolated and purified by various chromatographic methods, and their structures were identified by NMR and MS data analysis. Results: Thirty-four compounds were isolated and identified as 3β-acetoxy-12β-hydroxy-20(R), 25-epoxydammarane (1), 3β, 6α-diacetoxy-12β-hydroxy-20(R), 25-epoxydammarane (2), 3β-acetoxy-6α, 12β-dihydroxy-20(R), 25-epoxydammarane (3), 20(R)-panaxadiol (4), isodehydroprotopanaxatriol (5), 3-oxo-6α, 12β-dihydroxy-20(R), 25-epoxydammarane (6), dammar-(E)-20(22)-ene-3β, 12β, 25-triol (7), 6α-acetoxy-3β, 12β-dihydroxy-20(R), 25-epoxydammarane (8), 20(S)-protopanaxadiol (9), 20(R)-protopanaxadiol (10), 20(S)-25-ethoxyl-dammarane-3β, 12β, 20-triol (11), 20(R)-panaxatriol (12), dammar-(E)-20(22), 24-diene-3β, 6α, 12β-triol (13), 27-demethyl-(E, E)-20(22), 23-dien-3β, 12β-dihydroxydammar-25-one (14), 3β, 12β-dihydroxy-22, 23, 24, 25, 26, 27-hexanordamaran-20-one (15), 3β-acetoxy-6α, 12β, 25-trihydroxy-20(S), 24(R)-epoxy-dammarane (16), 20(S)-25-ethoxyl-dammarane-3β, 12β, 20-triol (17), dammar-(E)-20(22)-ene-3β, 6α, 12β, 25-tetrol (18), dammar-(Z)-20(22)-ene-3β, 6α, 12β, 25-tetrol (19), 20(S)-dammarane-3β, 12β, 20, 25-tetrol (20), 20(R)-dammarane-3β, 12β, 20, 25-tetrol (21), 20(S)-protopanaxatriol (22), 20(R)-protopanaxatriol (23), (20S, 24S)-dammarane-20, 24-epoxy-3β, 6α, 12β, 25-tetraol (24), (20S, 24R)-dammarane-20, 24-epoxy-3β, 6α, 12β, 25-tetraol (25), (20R, 24R)-dammarane-20, 24-epoxy-3β, 6α, 12β, 25-tetraol (26), 3β, 6α, 12β-trihydroxy-22, 23, 24, 25, 26, 27-hexanordamaran-20-one (27), 12β-hydroxy-20(R), 25-epoxydammarane-3β-O-β-D-glucopyranoside (28), 20(S)-dammarane-3β, 6α, 12β, 20, 25-pentol (29), 20(R)-dammarane-3β, 6α, 12β, 20, 25-pentol (30), 20(R)-dammarane-3β, 6α, 12β-trihydroxy-20, 25-epoxy-6-O-β-D-glucopyranoside (31), pseudo-ginsenoside-Rh2 (32), 20(S)-ginsenoside-Rh1 (33), and 20(R)-ginsenoside-Rh1 (34). Conclusion: Compounds 1-3, 6, 8, 11, 17, 24-26, and 32 are ginseng triterpenoids isolated from the acid hydrolysates of total saponins from the stems and leaves of P. ginseng for the first time. Pseudo-ginsenoside-Rh2 is a potent antiproliferative agent against human cancer cells.

Down-regulation of transcription factor PU.1 via abnormal epigenetic modification in chronic myeloid leukemia / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To investigate the underlying mechanism and clinical significance of PU.1 down-expression in chronic myeloid leukemia (CML) patients.</p><p><b>METHODS</b>Different methylation status of PU.1 promoter region containing 20 CpG islands in normal individuals, CML chronic phase and blast crisis patients, complete cytogenetic remission patients after imatinib treatment, and blast crisis bone marrow K562 CML cells was detected by bisulfite sequencing. Semi-quantitative PCR was used to detect the PU.1 mRNA expression in normal controls, CML chronic phase and blast crisis patients, and blast crisis bone marrow K562 CML cells. Indirect immune fluorescence and Western blot were used to analyze the exprtession of PU.1 protein in normal individuals, CML chronic phase and blast crisis patients, and blast crisis bone marrow K562 CML cells.</p><p><b>RESULTS</b>Aberrant methylation in the promoter region of transcription factor PU.1 was found in both CML chronic phase and blast crisis phase bone marrow cells, as well as in CML blast K562 cells. Down-expression of PU.1 mRNA and protein levels was found in above cells. No methylation in the promoter region of PU.1 was observed in normal individuals, and the PU.1 mRNA and protein expressions were not reduced at all. Furthermore, high methylation status of bone marrow cells was even observed in the CML patients who acquired complete cytogenetic remission.</p><p><b>CONCLUSIONS</b>The results of our study indicate that the epigenetic modification of PU.1 in CML patients and K562 cell line might be responsible for the down-expression of PU.1. The data suggest that aberrant methylation of PU.1 plays a role in CML pathogenesis, therefore, it might serve as a useful biomarker and potential target in therapy for chronic myeloid leukemia.</p>

Youchasaponin induces apoptosis of human leukemia Jurkat cells in vitro and its possible mechanism / 肿瘤

Objective: To investigate the apoptosis of human leukemia Jurkat cells induced by Youchasaponin in vitro and to explore its possible mechanism. Methods: The effects of Youchasaponin with different concentrations on the proliferation of Jurkat cells were detected by cell count assay. The cell cycle distribution and the apoptosis rate of Jurkat cells were determined by flow cytometry (FCM). The expression levels of caspase-3, poly (ADP-ribose) polymerase (PARP), p-Bcl-2, Bcl-2, Bax and caspase-9 proteins were analyzed by Western blotting. Results: The proliferation of Jurkat cells was significantly inhibited after treatment with Youchasaponin (1-16 μg/mL) in a dose-dependent manner. The percentage of Jurkat cells at G0/G1 phase and G2/M phase was decreased after treatment with Youchasaponin (1-4 μg/mL) for 24 h, while the percentage of Jurkat cells at S phase was increased. The apoptosis rate of Jurkat cells induced by Youchasaponin was increased in a dose-dependent manner. The expression levels of p-Bcl-2 and Bcl-2 proteins were down-regulated, and the expression levels of caspase-3, PARP and caspase-9 proteins were up-regulated, whereas the expression level of Bax protein had no change. Conclusion: Youchasaponin can inhibit the cell proliferation and induce the apoptosis of human leukemia cells. This effect may be related to the mitochondrial pathway of apoptosis. Copyright© 2011 by TUMOR.

Effects of amlodipine plus telmisartan or amlodipine plus amiloride regimen on blood pressure control in hypertensive patients: preliminary report of Chinese Hypertension Intervention Efficacy (CHIEF) trial / 中华心血管病杂志

<p><b>OBJECTIVE</b>To evaluate the effects of amlodipine-based antihypertensive combination regimen on blood pressure control and impact on cardiovascular events.</p><p><b>METHODS</b>From Oct. 2007 to Oct. 2008, a total of 13 542 hypertensive patients from 180 centers in China were included in this multi-centre randomized, controlled, blind-endpoint assessment clinical trial. Inclusion criteria were: essential hypertension, 50 - 79 years of age with at least one cardiovascular risk factor and signed consent forms. Patients were randomly assigned to receive low-dose amlodipine + diuretics (group A) or low-dose amlodipine + telmisartan (group T). The primary endpoints are composite of non-fatal stroke/myocardial infarction and cardiovascular death. All patients will be followed-up for 4 years.</p><p><b>RESULTS</b>The characteristics of patients between the two groups were similar: mean age (61.5 +/- 7.7) Yrs with 19% history of cerebrovascular diseases, 12% coronary diseases, 18% diabetes, 42% dyslipidemia, mean initial blood pressure 157/93 mm Hg. After 8-week treatment, mean blood pressure in group A and B were reduced to (133.0 +/- 11.0)/(81.0 +/- 7.6) mm Hg, (132.9 +/- 11.6)/(80.6 +/- 7.9) mm Hg respectively. Blood pressure control rates reached 72.1% and 72.6% in group A and T, respectively.</p><p><b>CONCLUSION</b>Amlodipine-based antihypertensive combination regimens achieved satisfactory blood pressure control rate in patients with essential hypertension in this patient cohort.</p>