Aim:To observe the effects of stearic acid,a long-chain saturated fatty acidconsisting of 18 carbon atoms,on brain(cortical or hippocampal)slices insultedby oxygen-glucose deprivation(OGD),glutamate or sodium azide(NAN_3)in vitro.Methods:The activities of hippocampal slices were monitored by population spikesrecorded in the CA1 region,In vitro injury models of brain slice were induced by10min of OGD,1 mmol/L glutamate or 10 mmol/L NaN_3.After 30min of pre-incubation with stearic acid(3-30μmol/L),brain slices(cortical or hippocampal)were subjected to OGD,glutamate or NaN_3,and the tissue activities were evalu-ated by using the 2,3,5-triphenyltetrazolium chloride method.MK886 [5 mmol/L;a noncompetitive inhibitor of proliferator-activated receptor(PPAR-α)] or BADGE(bisphenol A diglycidyl ether;100μmol/L;an antagonist of PPAR-γ)were testedfor their effects on the neuroprotection afforded by stearic acid.Results:Viabilityof brain slices was not changed significantly after direct incubation with stearicacid.OGD,glutamate and NaN_3 injury significantly decreased the viability ofbrain slices.Stearic acid(3-30 μmol/L)dose-dependently protected brain slicesfrom OGD and glutamate injury but not from NaN_3 injury,and its neuroprotectiveeffect was completely abolished by BADGE.Conclusion:Stearic acid can protectbrain slices(cortical or hippocampal)against injury induced by OGD or glutamate.Its neuroprotective effect may be mainly mediated by the activation of PPAR-γ. Aim: To observe the effects of stearic acid, a long-chain saturated fatty acidconsisting of 18 carbon atoms, on brain (cortical or hippocampal) slices insultedby oxygen-glucose deprivation (OGD), glutamate or sodium azide (NAN_3) in vitro. Methods : The activities of hippocampal slices were monitored by population spikesrecorded in the CA1 region, In vitro injury models of brain slices were induced by 10min of OGD, 1 mmol / L glutamate or 10 mmol / L NaN3.After 30min of pre-incubation with stearic acid (3-30 μmol / L), brain slices (cortical or hippocampal) were subjected to OGD, glutamate or NaN_3, and the tissue activities were evaluated- ated by using the 2,3,5-triphenyltetrazolium chloride method. MK 886 [5 mmol / L; a noncompetitive inhibitor of proliferator-activated receptor (PPAR-α)] or BADGE (bisphenol A diglycidyl ether; 100 μmol / L; an antagonist of PPAR- γ) were tested for their effects on the neuroprotection afforded by stearic acid. Results: Viabilityof brain slices was not changed significantly after direct incubat ion with stearicacid. OGD and glutamate injury but not from NaN_3 injury, and its neuroprotective effect was completely abolished by OGD and glutamate injury but not NaN_3 injury BADGE.Conclusion: Stearic acid can protectbrain slices (cortical or hippocampal) against injury induced by OGD or glutamate. Its neuroprotective effect may be mainly mediated by the activation of PPAR-γ.