Objective:To study the effect of atorvastatin calcium on the neurological function of rats with non-cardiac ischemic stroke and its mechanism.Methods:Thirty SD rats were randomly divided into sham operation group，model group and atorvastatin group，with 10 in each group. Non-cardiac ischemic stroke models were established for rats in the model group and the atorvastatin group. The rats in the atorvastatin group were given continuous intragastric administration of atorvastatin(1 mg·kg-1·d-1)for 2 w. For the sham operation group, the internal carotid artery was not blocked，and the sham operation group and the model group were given continuous intragastric administration of an equal volume of 0.9% sodium chloride solution. Observe the differences in various indicators such as neural function assessment，brain tissue pathological changes，neuronal apoptosis，and serum inflammatory factor levels(IL-6，TNF-αand IL-1β)among the groups，and Western blotting method to observe each group different expressions of rat neuronal apoptosis-related protein TLR4，nuclear transcription factor NF-κB p65，pIκB，Cleaved Caspase-3.Results:The neurological deficit score，HE staining pathological section observation，apoptosis rate，serum IL-6，TNF-αand IL-1βin the atorvastatin group were significantly improved compared with the model group(P<0.05). Western blotting showed that TLR4，NF-κB p65，p-IκB，and Cleaved Caspase-3 in the atorvastatin group were significantly down-regulated compared with the model group(P<0.05).Conclusion:Atorvastatin calcium inhibits T L R 4 a n d n u c l e a r t r a n s c r i p t i o n f a c t o r N F -κB p 6 5，i n h i b i t s n e u r o n a l a p o p t o s i s i n r a t s w i t h n o n - c a r d i a c ischemic stroke and improves neurological dysfunction through this pathway.