Abstract: Objective To study the role of reactive oxygen species (ROS) -mediated oxidative stress and pyroptosis in the cerebral ischemia-reperfusion (I/ R) injury in rats. Methods Adult male SD rats were divided into 5 groups as follows: the sham group, the I/ R group, the ROS scavenger N-acetylcysteine low dose (NAC-L) group, the NAC medium dose (NAC-M) group and the NAC high dose (NAC-H) group. The cerebral I/ R injury model was established and 50, 100 and 200 mg / kg NAC were injected intraperitoneally before ischemia and reperfusion as an intervention. The neurological function was evaluated 24 h after reperfusion, the percentage of cerebral infarction area, and the levels of ROS, malondialdehyde (MDA), 4-hydroxynonenal (4-HNE) and total antioxidant capacity (T-AOC) were measured. The expression levels of cleaved caspase-1 and N-terminal of gasdermin D (GSDMD-N) were detected. Results In the I/ R group, the percentage of cerebral infarction area, the amount of ROS, MDA, 4-HNE, and the expression levels of cleaved caspase-1 and GSDMD-N were significantly increased, while the amount of T-AOC was significantly decreased (P< 0. 05). In the NAC-L, NAC-M and NAC-H groups, the percentage of cerebral infarction area, the amount of ROS, MDA, 4-HNE, and the expression levels of cleaved caspase-1 and GSDMD-N were significantly decreased, while the amount of T-AOC was significantly increased (P< 0. 05). The changes of the above indexes became more obvious with the increase of the NAC dose. Conclusion ROS mediated oxidative stress and pyroptosis are involved in the cerebral I/ R injury in rats.

Key words: cerebral ischemia-reperfusion injury, reactive oxygen species, N-acetylcysteine; oxidative stress, pyroptosis