Fig. 10

Schematic representation of the effects of FFA on post-CA brain injury. After cardiac arrest and cardiopulmonary resuscitation, the BBB is compromised due to ischemia/reperfusion, and microglia/macrophages switch toward the pro-inflammatory functional status. Both BBB breakdown and pro-inflammatory microglia/macrophages polarization form a vicious cycle 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 accelerate neuroinflammation resolution, and further mitigates neuronal injury, thus ultimately improving survival and neurologic outcome. Neuroprotection occurs at least in part through the 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