Protective effect of NEP on Abeta-induced apoptosis in PC12 cells / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To identify the effect of NEP on Abeta -induced apoptosis in PC12 cells.</p><p><b>METHODS</b>PC12 cells that stably express NEP is generated and the effect of NEP on the process of apoptosis induced by Abeta is analyzed, including the viability of the cells, the production of LDH, ROS and ATP, the activity of Caspase-3.</p><p><b>RESULTS</b>NEP could improve the viability of cells and the production of ATP, inhibit the release of LDH and ROS. In the same time, the activity of caspase-3 descended (P < 0.05). But iNEP had not significant effect on cells apoptosis (P > 0.05).</p><p><b>CONCLUSION</b>NEP has the protective effect on Abeta-induced apoptosis in PC12 cells.</p>

Mechanism of reactive oxygen species in manganese chloride-induced apoptosis in PC12 cells / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To explore the mechanism of reactive oxygen species (ROS) in manganese chloride (MnCl(2))-induced apoptosis in PC12 cells.</p><p><b>METHODS</b>The model that MnCl(2) induced apoptosis in PC12 cells was established. The apoptotic effect of MnCl(2) on PC12 cells was analyzed with the MTT, the flow cytometry and the DNA fragmentation. The production of ROS and ATP in MnCl(2)-induced apoptosis of PC12 cells was examined. The influence of MnCl(2) on the expression of bcl-xl, bax and the activity of Caspase 3 was also analyzed.</p><p><b>RESULTS</b>MnCl(2) triggered PC12 cells apoptosis in a dose-and time-dependent manner (P < 0.01). The rate of apoptosis was significantly increased (P < 0.01) when MnCl(2) of 2 mmol/L induced PC12 cells for 36 hours. The production of ROS was increased (P < 0.001) and the quantity of ATP was decreased (P < 0.01) in PC12 cells with the same inducement of MnCl(2). The expression of bcl-xl was inhibited and the bax was activated in this process (P < 0.01). Caspase 3 was also activated (P < 0.01).</p><p><b>CONCLUSION</b>MnCl(2) induces apoptosis of PC12 cells, which is related to the increase of ROS, the inhibition of the mitochondria and the activation of Caspase 3.</p>