To investigate the brain protective effects and mechanism of urinary kallidinogenase (UK) in rabbits with post-cardiac arrest syndrome (PCAS). Methods: Japanese white rabbits were random divided into the sham group (n=6), PCAS group (n=12), UK high-dose group (UK-H group , n=12), and UK low-dose group (UK-L group, n=12). PCAS models were established by using asphyxia-induced cardiac arrest; the sham group was not subjected to asphyxia. Immediately after ROSC, UK-H and UK-L groups were given 17.5×10-3 PNAU/kg and 3.5×10-3 PNAU/kg doses of UK, and the PCAS group was injected with an equal amount of saline. Serum level of neuron specificity enolization enzyme (NSE) was examined before ROSC and 6 h, 24 h, and 48 h after ROSC respectively. Functional outcomes were measured by neurological deficit score. Rabbit brain tissue was collected after 48 h, and Western blot was performed to determine brain tissue Caspase-3 and Caspase-9 expression. Results: Compared to the sham group，serum level of NSE was significantly elevated in the PCAS group, UK-L group, and UK-H group 6 h, 24 h, and 48 h after ROSC (P<0.01). Compared to PCAS group，serum level of NSE and neurological deficit score was clearly decreased in the UK-L group and UK-H group 24 h and 48 h after ROSC; the expression level of Caspase-3 and Caspase-9 was significantly attenuated in the two groups 48 h after ROSC (P<0.05), with the UK-H group showing a greater reduction than the UK-L group (P<0.05). Conclusion: UK reduced brain inflammation and alleviated neurological deficit, and the mechanism may be related to inhibition of apoptosis