following CA/CPR
After transient global cerebral ischemia and reperfusion induced by
CA/CPR, delayed neuronal injury occurs
in
selectively vulnerable regions, such as the hippocampal CA1 [33].
Therefore, we conducted immunofluorescence staining to observe neuronal
loss among different groups. Results showed that the number of surviving
neurons stained by NeuN was significantly reduced in the vehicle group
compared with sham group, and this neuronal loss was substantially
mitigated by FFA treatment (Fig. 3A, B). Additionally, CA/CPR could lead
to widespread injury to neuronal dendrites, evidenced by obviously
decreased MAP2 immunostaining compared to sham group, and this dendritic
injury was partly averted by FFA treatment (Fig. 3A, B).
Microglia and astrocytes play a paramount role in orchestrating the
neuroinflammatory response. They are activated and migrate to the injury
site and thereby cause delay neuron loss following CA/CPR. As
illustrated, significantly more Iba1-positive microglia and
GFAP-positive astrocytes were detected in the vehicle group (Fig. 3A,
B), indicating neuroinflammation was activated in the brain after CA/CPR.
On the other hand, FFA treatment notably suppressed the activation of
microglia and astrocytes compared with the vehicle group (Fig. 3A, B).
Together, FFA treatment markedly attenuated histological impairment in
post-CA mice.