Conclusion
The results suggest that XSF can reduce the cytotoxicity of HBMEC induced by Aβ25-35, inhibit apoptosis, and regulate the transport of Aβ on BBB and energy metabolism disorder in HBMEC.
Methods
HBMEC cells were treated with Aβ25-35 to established neurotoxic cell model. After that, the cells were treated with 125, 250, 500 μg/mL XSF to observe the protective effect. The viability of HBMEC cells were evaluated by MTT assay, the Aβ25-35-induced apoptosis was characterized by Hoechst-33258 and the activity of cysteinyl aspartate specific proteinase-3. The expression level of Aβ1-42 in cells induced by Aβ25-35 was measured by human Aβ1-42 kit. Protein and mRNA expression levels of advanced glycation end products (RAGE), low density lipoprotein receptor-related protein 1 (LRP1), glucose transporter 1 and 3 (GLUT1 and GLUT3) were assayed by capillary electrophoresis immunoassay and quantitative real-time polymerase chain reaction analyses.
Results
In Aβ25-35 induced neurotoxic cells, the percentage of apoptotic cells, the concentration of Aβ1-42 and CASPASE-3 activity, protein and mRNA expression levels of RAGE increased significantly, but that of LRP1, GLUT1 and GLUT3 significantly decreased. XSF could inhibit the apoptotic of cells, reduced the concentration of Aβ1-42 and CASPASE-3 expression, downregulate RAGE and upregulate LRP1, GLUT1 and GLUT3 expression.