Objective To investigate the protective effect of H2S on neurological function in rats with acute cerebral infarction and the possible mechanism. Methods Totals of 48 healthy male SD rats were randomly divided into sham operation group， model group， saline group and H2S intervention group. The model of rat acute cerebral infarction was established by modified Longa method. 25 min before modeling， rats in the H2S intervention group were given intraperitoneal injection of NaHS 28 μmol/kg， while in the saline group were given the same amount of saline. After awakening and 72 h after operation， the neurological defects in rats of each group were evaluated. TTC staining was used to detect the cerebral infarct size in each group. TUNEL method was used to detect the cell apoptosis in brain tissue in each group. Western blot was used to detect the expressions of PI3K， p-PI3K， Akt， p-Akt， Bcl-2 and Bax proteins in the brain tissue. Results Compared with the model group and the saline group， the neurological defect score， the area of cerebral infarction and the apoptotic index in brain tissue in H2S intervention group were decreased， the differences were statistically significant（ P＜0.05）. Compared with the model group and the saline group， the relative expression levels of PI3K， Akt and Bcl-2 proteins in brain tissue in H2S intervention group were increased， while the relative expression levels of p-PI3K， p-Akt and Bax proteins were decreased， the differences were statistically significant（ P＜0.05）. Conclusions H2S might change the ratio of Bcl-2/Bax by inhibiting PI3K/Akt signaling pathway to reduce cerebral infarct size and apoptosis index and protect neurological function in rats with acute cerebral infarction.