Paeoniflorin inhibits growth of human colorectal carcinoma HT 29 cells in vitro and in vivo.
ABSTRACT The aim of the therapy of human malignancies is the inhibition of cell proliferation and/or induction of apoptosis. In present experiment, we investigated the in vitro and in vivo anticancer effects and associated mechanisms of paeoniflorin (PF), isolated from the paeony root, against colorectal cancer. In vitro, cell growth assay obviously showed the inhibition of tumor cell growth in a dose-dependent manner. Flow cytometry analysis showed that PF could mainly have the cell cycle arrest at G1, which is associated with DNA damage and activation of p53/14-3-3 zeta (ζ). The pro-apoptotic effect of PF was demonstrated by Annexin V-PI staining, and activation of caspase-3 and caspase-9 by Western immunoblotting. In vivo, the results showed that positive cells of PCNA in PF and docetaxel-treated group was decreased to 30% and 15% compared with control group of tumors, respectively. But apoptosis cells in PF- and docetaxel treated groups studied by TUNEL is increased to 40 ± 1.2% and 30 ± 1.5% compared with 24 ± 2.3% in negative control, respectively. Furthermore, the efficiency of tumor-bearing mice treated by PF was superior to docetaxel in vivo. Overall, PF may be an effective chemopreventive agent against colorectal cancer HT29, and the mechanism could be mediated via an regulation of p53/14-3-3ζ.
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ABSTRACT: Cordycepin is known to have many pharmacological effects such as anti-tumorigenic, anti-inflammatory and anti-angiogenic activity. However, cordycepin induced apoptosis through the DR3 pathway in human colon cancer cells has not been studied. The effect of cordycepin on anti-proliferation was investigated in this study. Cordycepin significantly inhibited cell viability in a dose and time-dependent manner. Cordycepin increased sub G1 and G2/M phase arrest on HT-29 cells at the concentration of 100μM, whereas cordycepin at 200μM and 400μM increased G1 phase arrest. Cordycepin induced apoptosis in HT-29 cells in a dose-dependent manner as detected by Hoechst and Annexin V-FITC staining. Intracellular ROS levels were higher in cordycepin treated cells as compared to control cells. The protein related to apoptosis was determined by antibody array. p53 and Bax expression increased treatment with cordycepin for 18h. DR3, caspase-8, caspase-1, cleaved caspase-3 and cleaved PARP expression increased. These finding suggest that the cordycepin induces apoptosis through the DR3 pathway in human colon cancer HT-29. These findings suggest that cordycepin should be evaluated further as a therapeutic agent in human colon cancer.Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 08/2013; · 2.99 Impact Factor
- Anti-cancer drugs 04/2013; 24(4):429. · 2.23 Impact Factor
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ABSTRACT: Isoprenoid and branched glycerol dialkanol diethers (iGDDs and bGDDs) have recently been found in marine and peat deposits, whereas their distribution and sources in soils are undetermined. We present the distributional characteristics of GDDs as well as their corresponding glycerol dialkyl glycerol tetraethers (GDGTs) in Chinese surface soils and a loess-paleosol sequence (LPS) in northwest China to study the source of GDDs and their relationship with GDGTs. The distributions of iGDDs and bGDDs are comparable with those of the corresponding GDGTs, with a dominance of iGDGTs over bGDGTs in alkaline soil and the opposite in acid soil. By extension, the GDD- and GDGT-based BIT indices exhibit the same trends in both surface soils and the LPS. The fractional abundances of individual iGDDs and bGDDs are also similar to those of the corresponding GDGTs, resulting in similar cyclization patterns for iGDGTs and iGDDs, and similar methylation indices for bGDGTs and bGDDs. These similarities indicate that bGDDs and iGDDs may share a common biological source with their corresponding GDGTs. In the LPS, the GDGT/(GDGT+GDD) ratio decreases exponentially with increased depth, which fits a first order kinetic degradation (or more specifically, transformation) model that has commonly been applied to other lipid classes; this is strong evidence for a diagenetic origin for GDDs. Although our results do not exclude production of GDDs directly by microorganisms, they do suggest that the GDDs may be the degradation products of GDGTs.Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 11/2013; · 2.99 Impact Factor