ABSTRACT
<p><b>OBJECTIVE</b>To investigate the mechanism of norcantharidin (NCTD)-induced SMMC-7721 hepatoma cell apoptosis.</p><p><b>METHODS</b>SMMC-7721 cell growth inhibition was measured by the MTT method. Apoptosis was detected by Annexin V/propidium iodide staining. The mitochondrial membrane potential was measured by flow cytometry. Western blot analysis was used to evaluate the level of cytochrome c, caspase-3, AIF, Bcl-2 and Bax expression.</p><p><b>RESULTS</b>NCTD inhibited SMMC-7721 cell growth in a time- and dose-dependent manner. The cells treated with NCTD showed the loss of mitochondrial membrane potential. The activities of caspase-3, cytochrome c, AIF, and Bax were up-regulated after NCTD treatment at different doses. The expression of Bcl-2 was decreased after treatment with NCTD.</p><p><b>CONCLUSIONS</b>NCTD could induce SMMC-7721 cell apoptosis. The activation of the mitochondrial pathway was involved in the process of NCTD-induced SMMC-7721 cell apoptosis.</p>
Subject(s)
Humans , Apoptosis , Apoptosis Inducing Factor , Metabolism , Blotting, Western , Bridged Bicyclo Compounds, Heterocyclic , Pharmacology , Caspase 3 , Metabolism , Cell Line, Tumor , Cytochromes c , Metabolism , Flow Cytometry , Liver Neoplasms , Metabolism , Pathology , Membrane Potentials , Mitochondria , Metabolism , bcl-2-Associated X Protein , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To review the research progress on Type IV secretion system (T4SS) in Helicobacter pylori.</p><p><b>DATA SOURCES</b>The data used in this review were identified by searching of PUBMED (1995 - 2007) online resources using the key terms 'Type IV secretion system' and 'Helicobacter pylori'.</p><p><b>STUDY SELECTION</b>Mainly original articles and critical reviews written by major pioneer investigators of this field were selected.</p><p><b>RESULTS</b>The research progress on T4SS in Helicobacter pylori was summarized. The structure and function was discussed.</p><p><b>CONCLUSIONS</b>T4SS is not only involved in toxin secretion and injection of virulence factors into eukaryotic host target cells, but also involved in horizontal DNA transfer to other bacteria and eukaryotic cells, through DNA uptake from or release into the extracellular milieu. It provides a new insight into the pathogenicity of Helicobacter pylori and a novel target for antimicrobials development. However, many challenges remain for us in understanding the biological role of T4SS in Helicobacter pylori.</p>