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.