Abstract: ObjectiveTo construct an apoptosis model of HT22 cells induced by inflammatory factors, so as to provide theoretical evidence for further exploration of the pathogenesis and anti-apoptosis of neuronal apoptosis induced by neuritis. MethodsBV2 mouse microglial cells and HT22 mouse hippocampal cells were selected in the current study. BV2 cells were exposed to 0.5 and 1.0 μg/ml of lipopolysaccharide (LPS) for 0, 6, 12 and 24 h and the levels of inflammatory factors, such as interleukin (IL) -1β and tumor necrosis factor (TNF) in the supernatant were detected. Then, the above supernatant was used to cultivate HT22 cells. The survival rate of HT22 cells were measured by CCK-8 assay. The apoptosis of HT22 cells were determined by Annexin Ⅴ. ResultsBV2 cells were able to secret IL-6, TNF, monocyte chemotactic protein-1 (MCP-1) and IL-10 after exposure to 0.5 and 1.0 μg/ml of LPS for 6, 12 and 24 h. The survival rate of HT22 cells were remarkably affected after exposure to the supernatant of BV2 cells induced by 1.0 μg/ml LPS for 24 h (P<0.05). After exposure for 12, 24 and 48 h, the survival rate of BV2 cells was decreased by 16.9%, 40.12% and 77.22%, compared with that before exposure. The apoptotic rate of HT22 cells was significantly higher after exposure to the supernatant of BV2 cells for 12, 24 and 48 h than that without exposure ( P<0.05 or P<0.001). ConclusionsExposure to HT22 cells for 24 h with the supernatant of BV2 cells induced by 1.0 μg/ml LPS for 24h can be used to mimic the neuronal apoptosis induced by neurogenic inflammation.