OBJECTIVETo investigate the protective effects of insulin-like growth factor-1 (IGF-1) on the nerve cells of neonatal rats under oxidative stress.

METHODSPrimary cortical neurons, oligodendrocytes, and astrocytes from newborn rats were cultured. An oxidative stress model was established with different concentrations of H2O2 (0-60 μmol/L); the degree of damage of nerve cells was evaluated by lactate dehydrogenase assay, and the viability of nerve cells was tested by MTT assay. An oxidative stress model was established with different concentration of H2O2 (0-80 μmol/L). Expression of Akt/p-Akt (Ser473) in neurons was measured by Western blot before and after IGF-1 (25 ng/mL) administration.

RESULTSCompared with those not treated with H2O2, the cortical neurons, oligodendrocytes, and astrocytes treated with different concentrations of H2O2 for 24 hours showed increased damage and decreased cell viability; compared with oligodendrocytes and astrocytes, neurons showed significantly more changes (P<0.01). Compared with those not treated with H2O2, the cortical neurons treated with different concentrations of H2O2 for 5 minutes showed a significant decrease in p-Akt (Ser473) level (P<0.01), which was dependent on the concentration of H2O2. For the neurons treated with low-concentration H2O2, the addition of IGF-1 could reverse the inhibition of Akt phosphorylation, eliminating the difference in p-Akt level compared with the neurons not treated with H2O2, (P>0.05); however, it had no significant effect on the inhibition of Akt phosphorylation by high-concentration H2O2, and the treated neurons still had a lower p-Akt level than untreated neurons (P<0.01 for all). For the cortical neurons that had been treated with different concentration of H2O2 for 1 hour, the addition of IGF-1 (25 ng/mL) could eliminate thedifference in p-Akt level between the treated neurons and untreated neurons (P>0.05).

CONCLUSIONSCortical neurons are more sensitive to oxidative stress induced by H2O2 than other nerve cells. IGF-1 has protective effects on cortical nerve cells under oxidative stress.