ABSTRACT
Objective To explore the effect of apolipoprotein E deficiency on astrocyte destruction in the ex vivo spinal cord slice model. Methods Vibratome-cut transverse spinal cord slices from C57BL/6 postnatal day 7 ApoE -/-mice and wild-type mice were cultured on transwell porous supports. After 7 days in the culture , spinal cord slices were exposed to LPS for 5 days. The expression of AQP4, GFAP and Iba1 was detected by immunofluorescence. The concentration of TNF-α and NO were detected by ELISA and method of nitrate reductase, respectively. Results Marked loss of AQP4 and GFAP staining were shown in LPS-affected groups, not in the control group, and the lesion score was higher in ApoE-/-group than WT-group (P<0.05). In addition, the expression of Iba1 and concentration of TNF-α, NO in the LPS-affected groups were more than that of the control group (P < 0.05), and they were higher in the ApoE-/-LPS group than the WT-LPS group (P < 0.05). Conclusions ApoE deficiency exacerbates astrocyte injury, likely through promoting the release of pro-inflammatory mediators from microglia.