Objective:To study the protective role of ischemic precondition in brain cells and its mechanism in rats after cerebral infarction.Methods:According to random number table method, 120 SD rats were divided into ischemic precondition group ( n=50), cerebral infarction group ( n=50), sham-operated group ( n=10), and normal control group ( n=10); cerebral infarction models of middle cerebral artery occlusion (MCAO) in the former two groups were induced by modified Longa thread method; precondition (blood flow in the middle cerebral artery was blocked for 15 min before model making) was given to the ischemic precondition group; rats in the sham-operated group were performed sham ischemic precondition and sham occlusion of middle cerebral artery blood; rats in the normal control group did not receive any treatment. At 24 h after model making, rats in the normal control group (n=10) and sham-operated group (n=10) were sacrificed, and 2, 6, 12, 24, and 48 h after model making, rats in the ischemic precondition group (n=10) and the cerebral infarction group (n=10) were sacrificed; the Caspase-3 expression in the ischemic penumbra was detected by immunohistochemistry, and the apoptosis rate in the ischemic penumbra was determined by TUNEL. Real-time PCR and Western blotting were used to detect the mRNA and protein expressions of arginyl-tRNA synthetase (ArgRS). Results:As compared with those in the normal control group and sham-operated group, the apoptosis rate, positive expression rate of Caspase-3, and ArgRs mRNA and protein expressions in the ischemic penomere zone of the rats in the cerebral infarction group were significantly increased at different time points after modeling ( P<0.05). As compared with those in the cerebral infarction group, the apoptosis rate, positive expression rate of Caspase-3, and ArgRs mRNA and protein expressions in the ischemic penomere zone at different time points after modeling in the ischemic precondition group were significantly decreased ( P<0.05). Conclusion:Cerebral ischemic precondition can inhibit the mRNA and protein expressions of ArgRS and Caspase-3 expression, reduce the apoptosis of brain cells, and thus play a neuroprotective role in brain tissues.