Neuroprotective effects of stearic acid against toxicity of oxygen/glucose deprivation or glutamate on rat cortical or hippocampal slices
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 (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 min 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 μmol/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 μmol/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.
Keywords:
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 min 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 μmol/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 μmol/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.