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.