5 CONCLUSIONS
In summary, we for the first time thoroughly characterize the therapeutic potential of FFA in post-CA brain injury, including ameliorating BBB breakdown and consequential formation of cerebral edema, facilitating a shift of microglia/macrophages towards a neuroprotective phenotype, and ultimately mitigating histological injury and improving functional outcome. These protective effects of FFA are possibly related to inhibition of TRPM4. Our work delivers novel insights into the mechanism of FFA-induced neuroprotection against brain injury caused by CA/CPR, advancing the current treatments and extending the clinical application of FFA outside of its typical use for analgesia against pain. Although pharmacological inhibitors of TRPM4 have several issues, FFA appears to represent a multipotent and promising agent in the management of post-CA brain injury.