Neuroprotective effects of stearic acid against toxicity of oxygen/glucose deprivation or glutamate on rat cortical or hippocampal slices  

作　　者：Ze-jian WANG Guang-mei LI Wen-lu TANG Ming YIN 

机构地区：[1]School of Pharmacy, Shanghai Jiaotong University, Shanghai 200030, China

出　　处：《Acta Pharmacologica Sinica》2006年第2期145-150,共6页中国药理学报（英文版）

基　　金：Project supported by the Natural Science Foundation of Shanghai(№03ZR14056).

摘　　要：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 （NAN3） 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 10 min of OGD, 1 mmol/L glutamate or 10 mmol/L NaN3. After 30 rain of preincubation with stearic acid （3-30 μmol/L）, brain slices （cortical or hippocampal） were subjected to OGD, glutamate or NaN3, and the tissue activities were evaluated 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; 100 pmol/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 NaN3 injury significantly decreased the viability of brain slices. Stearic acid （3-30 pmol/L） dose-dependently protected brain slices from OGD and glutamate injury but not from NaN3 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.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 （NAN3） 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 10 min of OGD, 1 mmol/L glutamate or 10 mmol/L NaN3. After 30 rain of preincubation with stearic acid （3-30 μmol/L）, brain slices （cortical or hippocampal） were subjected to OGD, glutamate or NaN3, and the tissue activities were evaluated 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; 100 pmol/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 NaN3 injury significantly decreased the viability of brain slices. Stearic acid （3-30 pmol/L） dose-dependently protected brain slices from OGD and glutamate injury but not from NaN3 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.

关 键 词：fatty acid brain slices ISCHEMIA GLUTAMATE energy metabolism 

分 类 号：R338[医药卫生—人体生理学]