Polydatin induces human cervical cancer cell apoptosis via PI3K/AKT/mTOR signaling pathway / 中国中药杂志

To observe the effect of polydatin on proliferation and apoptosis of cervical cancer HeLa cells and explore its possible mechanism. The growth inhibitory effect was detected with MTT assay. After HeLa cells were treated with different concentrations (50, 100, 150 μmol•L⁻¹) of polydatin, MTT assay was used to detect the inhibitory effect of polydatin on proliferation of HeLa cells; Acridine orange/ethidium bromide staining was used for morphological changes in apoptotic HeLa cells； Annexin/propidium iodide staining was applied to detect HeLa cell apoptotic rate. In addition, flow cytometry was employed to analyze apoptosis and cell cycle distribution； RT-PCR and Western blot assay were used to detect PI3K, AKT, mTOR, and P70S6K mRNA and protein expression levels. The results showed that polydatin significantly inhibited HeLa cells proliferation in a dose-dependent manner. Polydatin can cause S phase arrest for HeLa cells, promote cell apoptosis and decrease the mRNA and protein expression levels of PI3K, AKT, mTOR and P70S6K. It indicated that polydatin could inhibit proliferation and induce apoptosis of cervical cancer HeLa cells, and the mechanism may be associated with inhibiting the PI3K/AKT/mTOR signaling pathway and suppressing downstream gene expression.

An investigation of clinical features and immunological functions of HCV-specific cytotoxic T lymphocytes in HIV/HCV co-infected patients / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To investigate the clinical features, CD4+ T and CD8+ T cell counts, HIV RNA load, HCV RNA load, CD8+ T cell responses to HCV of HIV/HCV co-infected and HCV mono-infected patients and to assess the mutual influences of the two viruses in the infection.</p><p><b>METHODS</b>Fifty-nine patients with HIV/HCV co-infection were enrolled in this study. Thirty-six patients with HCV mono-infection served as a comparison group. The liver function, peripheral blood CD4+ T and CD8+ T cell counts, HIV RNA load and HCV RNA load were compared between the groups. Peripheral blood mononuclear cells were analyzed by interferon-gamma ELISpot using a panel of HCV antigens.</p><p><b>RESULTS</b>The frequency of HIV/HCV co-infection in those blood donors in Henan, China was 60.8%. ALT and AST in the HIV/HCV co-infection patients were not different from those of the HCV group. Globulin in the HIV/HCV co-infection group was higher than that in the HCV group (P<0.01). CD4+ T cell counts in the HIV/HCV co-infection group were lower than those in the HCV group, but CD8+ T cell counts in the HIV/HCV co-infection group were higher than those in the HCV group (P<0.01). The HCV RNA loads were higher in the HIV/HCV co-infection group than in the HCV group(P<0.01). The magnitude of HCV-specific CTL response to HCV-NS3 overlapping peptides in the HIV/HCV co-infection group (649.34+/-685.90) was higher than that in the HCV group (1233.70+/-1085.16). Albumin was negatively correlated with HCV RNA (log10copies/ml) in the HIV/HCV co-infection group (r=-0.540). A positive correlation was found between platelet and peripheral blood CD4+ T cell counts (P<0.05). No linear correlation was found between HCV virus loads, HIV virus loads or peripheral blood CD4+ T cell counts.</p><p><b>CONCLUSION</b>The frequency of HIV/HCV co-infection in the blood donors in Henan, China was 60.8%. HIV/HCV co-infection aggravated the progress of chronic hepatitis C.</p>