Stearic acid protects primary cultured cortical neurons against oxidative stress

Aim:To observe the effects of stearic acid against oxidative stress in primarycultured cortical neurons.Methods:Cortical neurons were exposed to glutamate,hydrogen peroxide(H2O2),or NaN3insult in the presence or absence of stearicacid.Cell viability of cortical neurons was determined by MTT assay and LDHrelease.Endogenous antioxidant enzymes activity[superoxide dismutases(SOD),glutathione peroxidase(GSH-Px),and catalase(CAT)] and lipid peroxidation incultured cortical neurons were evaluated using commercial kits.{3-[l(p-chloro-benzyl)-5-(isopropyl)-3-t-butylthiondol-2-yl]-2,2-dimethylpropanoic acid,Na}[MK886;5 μmol/L;a noncompetitive inhibitor of proliferator-activated receptor(PPAR)α],bisphenol A diglycidyl ether(BADGE;100 μmol/L;an antagonist ofPPARγ),and cycloheximide(CHX;30 μmol/L,an inhibitor of protein synthesis)were tested for their effects on the neuroprotection afforded by stearic acid.Western blotting was used to determine the PPARγprotein level in cortical neurons.Results:Stearic acid dose-dependently protected cortical neurons againstglutamate or H202 injury and increased glutamate uptake in cultured neurons.This protection was concomitant to the inhibition of lipid peroxidation and to thepromotion activity of Cu/Zn SOD and CAT in cultured cortical neurons.Itsneuroprotective effects were completely blocked by BADGE and CHX.Afterincubation with H202 for 24 h,the expression of the PPARγprotein decreasedsignificantly(P<0.05),and the inhibitory effect of H2O2on the expression of PPARγcan be attenuated by stearic acid.Conclusion:Stearic acid can protect corticalneurons against oxidative stress by boosting the internal antioxidant enzymes.Its neuroprotective effect may be mainly mediated by the activation of PPARγandnew protein synthesis in cortical neurons.