Effect of IL-1β on expression of SNAP-25 in the hippocampus in septic neonatal rats

Abstract

Objective To investigate the effect of interleukin-1β (IL-1β) on the expression of synaptic protein SNAP-25 in the hippocampus in septic neonatal rat induced by systemic lipopolysaccharide (LPS) injection. Methods Sprague-Dawley (SD) rats were randomly divided into two groups: control group and sepsis group. The rat model of sepsis was produced by intraperitoneal injection of 1 mg/kg LPS, and rats in the control group were injected with an equal volume of 0.01 mol/L phosphate buffered saline (PBS). The expression levels of IL-1β and IL-1R1 in the hippocampus at 1, 2 and 3 d, and synaptosomal-associated protein 25 (SNAP-25) at 7, 14 and 24 d after LPS intraperitoneal injection were detected by Western blot. After cultured for 24 h, primary hippocampal neurons were divided into four groups including the control group, IL-1β (40 ng/mL) treatment group, IL-1β (40 ng/mL) + IL-1Ra (40 ng/mL) treatment group, and IL-1Ra (40 ng/mL) treatment group. The effect of IL-1β on SNAP-25 expression in primary hippocampal neuron was determined by Western blot and real-time PCR. The purity of hippocampal neurons were identified by NeuN immunofluorescence staining and the activity of neurons were detected by CCK-8 assay. All data were analyzed by SPSS version 22.0. The data were analyzed by student-t test and Dunnett-t test. The interaction effects were analyzed by factorial ANOVA. Differences were considered to be statistically significant if P< 0.05. Results Compared with the control group, the expressions of IL-1β and IL-1R1 were significantly increased in the hippocampus at 1, 2 and 3 d after intraperitoneal injection of LPS (P 0.05). Conclusions IL-1β may possibly inhibit the expression level of SNAP-25 protein in the hippocampus in the septic rats through its receptor IL-1R1, which would contribute to cognitive dysfunction of septic neonatal rats in later life. Key words: IL-1β; Sepsis; SNAP-25