ABSTRACT
Aim To study the influences of miR-203 on ursolic acid (UA ) sensitivity in leukemic K562 cell.Methods In the experimental system,eukaryot-ic expression vector of hsa-miR-203 (PmiR-203 )was transfected into K562 cells using LipofectamineTM 2000.K562 cells were incubated with different con-centration of UA alone or in combination with PmiR-203 .The cell proliferation was analyzed by MTT as-say.The cell apoptosis was measured by double stai-ning with Annexin V and Propidium Iodide.The ex-pression of Bcr/abl protein was detected by Western Blot.Results The miR-203 promoted the sensitivity of UA by up to 1 .55-fold and the IC50 was reduced from 44.3μmol · L-1 to 30.7 μmol · L-1 .The a-mount of apoptotic cells was increased in UA combined with PmiR-203 group (P<0.05).PmiR-203 downreg-ulated the expression of Bcr/abl protein in K562 cells. Conclusion Our results support a substantial role of miR-203 that enhances UA sensitivity in K562 cell and the mechanism appears to be related to the dounregula-tion of Bcr/abl by miR-203 .
ABSTRACT
@#Objective To explore the mechanism of the Jiedu Huayu Ⅱ Decoction in actue hepatic failure.MethodsThe acute hepatic failure rat models were induced with thioacetamide (TAA).84 SPF Wistar rats were divided into 7 groups randomly:blank group,model group,low dose group,middle dose group,high dose group,lactulose group,and the Angong Niuhuang Pill group.The drugs were administrated by gavage 3 d before model-making,5.5 d in total.The expression of Bcl-2,cytochrome C in mitochondrial and cytoplasm were measured with Western Blot.ResultsThe expression of Bcl-2 reduced in mitochondrial,the expression of cytochrome C increased in cytoplasm and reduce in mitochondrial in model group compare with that of blank group.Jiedu Huayu Ⅱ Decoction was able to enhance the expression of Bcl-2 and restrain cytochrome C release from mitochondrial to cytoplasm.Moreover,it shows dose-effect relation.ConclusionThe protection of Jiedu Huayu Ⅱ Decoction for hepatocyte in acute hepatic failure rats maybe relate to the increase of Bcl-2 in mitochondrial,blocking the mitochondrial permeability transition pore to arrest cytochrome C releasing.
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Objective To observe the toxicity, apoptosis and cell proliferation cycle of Mangiferin on the BEL 7404 human hepatocellular carcinoma cell line, and explore the possibility of Mangiferin as a new tumor chemopreventive drug. Methods MTT method was used to determine the effect of Mangiferin on cell proliferation, microscopy method was used to observe cytotoxicity of Mangiferin, and flow cytometry method was used to determine apoptosis induction and cell cycle proliferation blocking effects of Mangiferin. Results The cytotoxicity effects were observed in various concentrations of Mangiferin and at different exposure times. The effects were enhanced as the Mangiferin concentration increased and exposure time prolonged. The apoptosis effect was also enhanced, and cell cycle arrested at G 2/ M phase. All the above effects became significant when cells exposed to the concentration from 20 ?mol/L to 200 ?mol/L of Mangiferin at 24 h. Conclusions Mangiferin is cytotoxic, and may induce apoptosis. Mangiferin has cell cycle blocking effects on hepatocellular carcinoma cells. Its pharmaceutical potentials is worth for further investigating.