Figure 1.

Neuroprotective effect of PMA against H₂O₂-induced toxicity on rat primary neurons. Rat primary neurons were exposed to oxidative stress injury induced by H₂O₂ (75 μM), and neuron survival was estimated 24 h after the beginning of the experiment (A and B). Concentration-dependent biological effects of PMA were observed against H₂O₂ toxicity when PMA was added 24 h before exposure of H₂O₂ on hippocampal (A) and cortical (B) neurons. In C, hippocampal neurons were pretreated with PMA (0.1 and 1.0 μM) before the addition of different concentrations of H₂O₂ (30, 100, and 300 μM). Western blot analysis showed the expression of PKC in hippocampal neuronal cultures after PMA treatment (D). (E) An inactive enantiomer of PMA, 4α-PMA, was added in the same conditions as for PMA. Hippocampal neurons were treated by using identical conditions as described above and 5.0 μM of the HO inhibitor (SnPPIX) was added at the same time as PMA. (F) The effect of a PKC inhibitor, bisindolylmaleimide, on the neuroprotective effect of PMA in hippocampal neuronal cultures.