〔Abstract〕 Objective To investigate the inhibitory effect of breviscapine(Bre) on pyroptosis and apoptosis of neuronal cells in chronic cerebral ischemia(CCI) rats by regulating the activation of NLRP3 inflammasome. Methods Male SD rats were randomly divided into sham group, 2 VO group, 2 VO+breviscapine(2.5, 5, 10 mg/kg) groups. The model of CCI was established by permanently ligating the bilateral common carotid arteries(2 VO) in rats. The learning and memory ability of rats were detected by Morris water maze test. The pathological changes and apoptosis of brain tissue were detected by HE and Tunel staining respectively. NLRP3, Caspase 1, interleukin(IL)-1β,IL-6 and cleaved Caspase-3 proteins expression levels were detected by Western blot. Results Compared with the sham group, the spatial learning and memory ability was disordered, the latency was significantly prolonged, the target quadrant dwell time and the number of crossing target quadrants significantly reduced in the 2 VO group rats(P<0.01). The apoptosis, degeneration and necrosis have been increased in cortical and hippocampal neurons in the 2 VO group rats. Also, the NLRP3 inflammasome in the hippocampus was activated, the expressions of Caspase 1, IL-6 and IL-1β protein were up-regulated, and Caspase-3 protein was activated, which further promoted neuronal apoptosis in the 2 VO group rats. Compared with the 2 VO group, Bre significantly reduced the latency of the platform found, increased the target quadrant residence time and the number of crossing target quadrants in rats. Bre reduced apoptosisand the pathological damage of cortical and hippocampal neurons, increased the number of neuronal cells, and improved neuronal cell morphology and alleviated nuclear pyknosis in CCI rats. In addition, Bre significantly inhibited the activation of NLRP3 inflammasome in hippocampus, down-regulated the expression of Caspase 1, IL-6 and IL-1β, inhibited neuronal apoptosis and the activation of Caspase-3 proteinand. Conclusion Bre can significantly improve the cognitive function of CCI rats, and reduce the pathological damage of ischemic neurons. The mechanism may be related to inhibiting the activation of NLRP3 and pyroptosis pathway.