Objective By observing the effect of acupuncture on apoptosis-associated Fas/FasL signaling pathway,to explore the effect of acupuncture on nerve damage in rats after ischemic stroke(IS).Method Sixty Sprague-Dawley(SD)rats were randomized into a control group,a model group,an acupuncture group,and a Nimodipine group with 15 mice in each group.The IS model was developed using the middle cerebral artery occlusion(MCAO)method.The acupuncture group was intervened by acupuncture at Baihui(GV20),Shuigou(GB26),Dazhui(GV14),Neiguan(PC6),and Sanyinjiao(SP6);the Nimodipine group was offered Nimodipine via intragastric administration;rats in the control and model groups only received routine feeding.The neurological deficit was scored in each group of rats;2,3,5-triphenyl tetrazolium chloride(TTC)staining was used to observe the cerebral infarction volume;neuronal damage was observed using Nissl staining;the TdT-mediated dUTP Nick-end labeling(TUNEL)technique was applied to detect neuronal apoptosis;immunohistochemistry was adopted to observe the expression of Fas and cysteine aspartate-specific protease-3(caspase-3);Western blot was applied to detect the protein expression of Fas,Fas ligand(FasL),caspase-3,and cysteine aspartate-specific protease-8(caspase-8).Result Compared to the control group,the neuronal cells shrank and arranged loosely in the model group rats,with a decrease in the Nissl body content and increases in the neurological deficit score,brain tissue water content,cerebral infarction volume,neuronal apoptosis rate,and protein expression of Fas,FasL,caspase-3,and caspase-8(P<0.05).Compared to the model group,the neuronal cell morphology improved in the acupuncture and Nimodipine groups,with an increase in the Nissl body content and significant decreases in the neurological deficit score,brain tissue water content,cerebral infarction volume,neuronal apoptosis rate,and protein expression of Fas,FasL,caspase-3,and caspase-8(P<0.05).Conclusion Acupuncture can improve nerve damage and neuronal apoptosis in rats after IS,and the mechanism may be associated with inhibiting the Fas/FasL signaling pathway.