The neonatal rat cerebral cortex AS were cultured and purified in vitro. The AS were randomly divided into control group， LPS group and LPS+carnosine groups （10，30，and 90 mmol·L^-1 carnosine ）.The cells in control group were only cultured with complete medium； the cells in LPS group were stimulated in vitro with 1 mg·L^－1 LPS for 24 h to construct the inflammatory injury model； the cells in LPS+carnosine groups were cultured with 10，30， and 90 mmol·L^－1carnosine， respectively； in complete medium for 1 h， then treated with LPS with a final concentration of 1 mg·L^－1 for 24 h.The survival rates of AS in various groups were determined by MTT assay. The levels of interleukin-1β（IL-1β） and tumor necrosis factor-α（TNF-α） in the AS culture medium were detected by ELISA. DCFH-DA fluorescence probe was used to detect the reactive oxygen species（ROS） levels in AS in various groups； Hoechst 33258 fluorescence staining was used to detect the apoptotic rates of AS in various groups. The expressions of phosphorylated nuclear transcription factor-κB p65（p-NF-κB p65） in the AS and the number of p-NF-κB p65 positive cells in various groups were determined by immunofluorescence staining. The expression levels of p-NF-κB p65 protein in the AS in various groups were detected by Western blotting method.

Compared with control group， the survival rate of AS in LPS group was significantly decreased（P<0.05）， the levels of IL-1β and TNF-α in AS culture medium were increased（P<0.05）， the ROS level in AS was significantly increased（P<0.05），the apoptotic rate and the number of p-NF-κB p65 positive AS were increased significantly（P<0.05），and the expression level of p-NF-κB p65 protein in the AS was increased（P<0.05）.Compared with LPS group， the survival rates of AS in LPS+carnosine groups were significantly increased（P<0.05）， the levels of IL-1β and TNF-α in AS culture medium were decreased（P<0.05）， the ROS levels in the AS were decreased（P<0.05）， the apoptotic rates and the number of p-NF-κB p65 positive AS were decreased significantly（P<0.05），and the expression levels of p-NF-κB p65 protein in the AS were decreased（P<0.05）.

Carnosine can inhibit the release of the inflammatory factors IL-1β and TNF-α in the AS induced by LPS， and its mechanism may be related to inhibiting the ROS production in AS induced by LPS and then inhibiting the activation of NF-κB p65.