Neuroprotective effects of stearic acid against toxicity of oxygen/glucose deprivation or glutamate on rat cortical or hippocampal slices
Tang Ming
Abstract
Tang Ming
Abstract
Aim:To observe the effects of stearic acid,a long-chain saturated fatty acid consisting of 18 carbon atoms,on brain(cortical or hippocampal)slices insulted by oxygen-glucose deprivation(OGD),glutamate or sodium azide(NAN_3)in vitro. Methods:The activities of hippocampal slices were monitored by population spikes recorded in the CA1 region,In vitro injury models of brain slice were induced by 10min 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 tested for their effects on the neuroprotection afforded by stearic acid.Results:Viability of brain slices was not changed significantly after direct incubation with stearic acid.OGD,glutamate and NaN_3 injury significantly decreased the viability of brain slices.Stearic acid(3-30 μmol/L)dose-dependently protected brain slices from OGD and glutamate injury but not from NaN_3 injury,and its neuroprotective effect was completely abolished by BADGE.Conclusion:Stearic acid can protect brain slices(cortical or hippocampal)against injury induced by OGD or glutamate. Its neuroprotective effect may be mainly mediated by the activation of PPAR-γ.
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Aim:To observe the effects of stearic acid,a long-chain saturated fatty acid consisting of 18 carbon atoms,on brain(cortical or hippocampal)slices insulted by oxygen-glucose deprivation(OGD),glutamate or sodium azide(NAN_3)in vitro. Methods:The activities of hippocampal slices were monitored by population spikes recorded in the CA1 region,In vitro injury models of brain slice were induced by 10min 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 tested for their effects on the neuroprotection afforded by stearic acid.Results:Viability of brain slices was not changed significantly after direct incubation with stearic acid.OGD,glutamate and NaN_3 injury significantly decreased the viability of brain slices.Stearic acid(3-30 μmol/L)dose-dependently protected brain slices from OGD and glutamate injury but not from NaN_3 injury,and its neuroprotective effect was completely abolished by BADGE.Conclusion:Stearic acid can protect brain slices(cortical or hippocampal)against injury induced by OGD or glutamate. Its neuroprotective effect may be mainly mediated by the activation of PPAR-γ.
Key concepts: Neuroprotection, Glutamate receptor, Stearic acid, Hippocampal formation, Chemistry, Pharmacology, Biochemistry, Endocrinology