Objective:To investigate the effects of butylphthalide on reducing neuronal apoptosis in rats with cerebral infarction by inhibiting the JNK / P38 MAPK signaling pathway. Methods:Forty-eight SD male rats were divided into DZ group (control group), CI group (model group) and NBP group (butylphthalide group). Rats in CI group and NBP group were used to establish cerebral infarction models. NBP group used NBP. The solution (80 mg / (kg ? d)) was administered orally, and the remaining two groups were administered with the same volume of peanut oil. After 14 consecutive days of treatment, the Zea Longa score was used to evaluate the neurological function of DZ, CI and NBP rats. Scoring, TTC staining was used to observe the cerebral infarction volume of rats in DZ group, CI group and NBP group, HE staining was used to observe the pathological morphology of brain tissue in DZ group, CI group and NBP group. Neuronal apoptosis, West blot was used to detect the expression of p-JNK and p-p38MAPK in brain tissues of DZ group, CI group and NBP group. Results:The neurological function of the rats in the CI group was higher than that in the DZ group, and the difference was statistically significant (P <0.05). The neurological function score of the rats in the NBP group was reduced compared with the CI group, and the difference was statistically significant (P <0.05). The cerebral infarction volume in the group was 35.56％ higher than that in the DZ group, and the difference was statistically significant (P <0.05). The minor infarct volume in the NBP group was 21.59％, which was less than that in the CI group, and the difference was statistically significant (P <0.05). Nerve cells are neatly sorted, with a large number. The gap between blood vessels and interstitial tissue in the CI group is enlarged, the cells are severely contracted, and the neuron structure is incomplete. Compared with the CI group, the NBP group has reduced neuron contraction and increased number; The dead nerve cells were brown. The apoptosis rate of nerve cells in the CI group was 79.65％ higher than that in the DZ group was 5.82％. The difference was statistically significant (P <0.05). The nerve cell apoptosis rate in the NBP group was 30.23％. Compared with CI group, the difference was statistically significant (P <0.05); West blot results showed that p-JNK and p-p38MAPK protein expression in CI group was higher than that in DZ group, and the difference was statistically significant (P <0.05). The levels of p-JNK and p-p38MAPK proteins in the NBP group were lower than those in the CI group. There was statistically significant (P <0.05). Conclusion:Butylphthalide can improve neurological damage, reduce apoptotic nerve cells, and reduce infarct volume in rats with cerebral infarction, which is related to the inhibition of JNK / P38 MAPK pathway expression.