RESUMO
To study the clinical efficacy and safety of different biliary drainages in malignant obstructive jaundice (MOJ) treatment. METHODS: 69 patients with MOJ admitted to our hospital from October 2016 to March 2019 were recruited as the study cohort and divided into an endoscopic retrograde cholangiopancreatography group (the ERCP group, n=38) and a percutaneous transhepatic cholangial drainage group (the PTCD group, n=31) according to the different drainage approaches each patient underwent. We compared the two groups' hepatic function indexes (total serum bilirubin (TB), alanine aminotransferase (ALT), and aspartate aminotransferase (AST)), their immune cells (CD3+ T cells, CD4+ T cells, and CD8+ T cells), surgical success rates, jaundice reduction response rates, and postoperative complications. RESULTS: The surgical success rates and the jaundice reduction response rates were similar in the two groups (P > 0.05). No statistically significant differences were observed in the hepatic function indexes or in the immune cells before and after treatment in the two groups (all P > 0.05). Moreover, all the indexes we measured were lower post-treatment than they were pre-treatment (TB, ALT, AST, and CD8+) except for the CD3+ and CD4+ levels (all P < 0.05). The incidence of postoperative complications in the ERCP group was significantly lower than the incidence in the PTCD group (P < 0.05). CONCLUSION: Both ERCP and PTCD can contribute to better clinical results in the treatment of MOJ, relieve obstructions effectively, improve hepatic function, and enhance immune function, but there are fewer complications after ERCP.
RESUMO
The present study investigated the mechanism of selective killing of liver cancer cells of melanoma differentiation associated gene-7 (MDA-7, also called IL-24α) in order to provide a theoretical basis for gene therapy of liver cancer. A recombinant eukaryotic expression vector (pcDNA3-MDA-7) containing human MDA-7 gene was constructed, which was then delivered to liver cancer cell line HepG2 and normal liver cell line L02. The positive cell clone was screened by G418. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was performed to confirm the occurrence of MDA-7 transcription in the transfected cells. The protein expression of MDA-7 was determined by western blot analysis. The effects of MDA-7 on liver cancer cell proliferation and apoptosis were investigated through MTT assay and flow cytometry by Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) double-staining. The mitochondrial protein was extracted from the normal liver cell line L02 and liver cancer cell line HepG2 at 3 day post-culture, in which the alterations of anti-apoptotic B-cell lymphoma-2 (Bcl-2), pro-apoptotic Bcl-2 associated X protein (Bax), mitochondria-released cytochrome c and caspase 9 were determined by western blot analysis. pcDNA3-MDA-7 mediated the expression of foreign gene MDA-7 in HepG2 and L02 cells. MDA-7 promoted liver cancer cell apoptosis and inhibited cell proliferation; while no effect was exerted on normal liver cells, as determined by the MTT assay and flow cytometry. Relative to the L02 cells, the protein expression of Bcl-2 was downregulated in the HepG2 cells, while that of Bax, cytochrome c and caspase 9 were upregulated. In the study, the eukaryotic expression vector pcDNA3-MDA-7 was successfully constructed, it can mediate the expression of MDA-7 in human liver cancer cells and normal liver cells and inhibits the proliferation of human liver cancer cells through the restored expression of mitochondrial pro-apoptotic Bcl-2.
