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This method provides BEZ235 a simple and effective way to analyse each of these biomolecules without affecting yield and quality. We also show that isolated biomolecules are of the highest purity and compatible for all the respective downstream applications, such as PCR amplification, RT��PCR (reverse transcription��PCR), real-time PCR, reverse Northern blotting, SDS/PAGE and Western blot analysis. The buffers and reagents used in this method are optimized extensively to achieve the cost effective and reliable procedure to separate the functional biomolecules of the cell. ""In order to investigate the effects of bone marrow-derived MSCs (mesenchymal stem cells) in reversing liver fibrosis and to determine their possible mechanism of action, mouse MSCs were infused into the tail vein of a CCl4 injection mouse chronic model. MSCs caused a 17-DMAG (Alvespimycin) HCl decrease in liver fibrosis histopathologically, 4 weeks after transplantation. The reduction in liver collagen was confirmed by quantitative analysis. Moreover, lipid peroxidation in the CCl4/MSC group decreased significantly. Quantitative RT (reverse transcription)-PCR analysis showed administration of MSCs has a significant antifibrotic effect as evidenced by the decrease in expression of liver collagen and increase in MMP13 (matrix metalloproteinase 13) in the CCl4/MSC group when compared with the CCl4 group, 4 weeks after transplantation. The expression of ��SMA (smooth muscle actin) and TIMP1 was also down-regulated in the CCl4/MSC group. Additionally, the expression of MMP9 was significantly up-regulated in the CCl4-treated group; however, there was no significant change after MSC injection. Few engrafted cells in the recipient liver and were able to differentiate into albumin-positive cells. In conclusion, MSCs can enhance recovery of a CCl4-injured mouse liver BLU9931 chemical structure through their influence in reducing collagen deposition by possibly affecting expression of MMPs. ""Cholangiocarcinoma is the second most common primary hepatic tumour originating from biliary tract epithelial cells with poor prognosis. Enhanced c-Myc protein expression contributes to many aspects of tumour cell biology. Although the ability of c-Myc to drive unrestricted cell proliferation and to inhibit cell differentiation had been well recognized, whether down-regulated c-Myc expression can inhibit tumour cell invasion still remains to be explored. The c-Myc ASODN (antisense oligodeoxyribonucleotide) and NSODN (nonsense oligodeoxyribonucleotide) were designed, synthesized and transfected into human QBC939 bile duct carcinoma cells using the Lipofectamine 2000 reagent. The protein expression of c-Myc was detected by Western blot. A transwell experiment was applied to evaluate the invasive capacity of the QBC939 cells. c-Myc ASODN could significantly suppress the c-Myc protein expression (P