Figure 11. Schematic representation of the effects of FFA on
post-cardiac arrest brain injury.
After cardiac arrest and
cardiopulmonary resuscitation, BBB is compromised due to
ischemia/reperfusion, and
microglia/macrophages
switch towards the pro-inflammatory functional status. Both BBB
breakdown and pro-inflammatory microglia/macrophages polarization form a
vicious circle contributing to enlarge brain injury continuously. FFA
treatment effectively alleviates BBB breakdown, modifies the functional
status of microglia/macrophages to enhance the removal of cellular
debris and speed neuroinflammation resolution, and further mitigates
neuronal injury, thus ultimately improving survival and neurologic
outcome. The neuroprotection is at least in part through modulation of
the TRPM4 channel in the neurovascular unit. To sum up, FFA may stand
out as a multipotent candidate drug for addressing brain injury
resulting from cardiac arrest and cardiopulmonary resuscitation.