[Protective effect of ß-asarone on PC12 cells injury induced by Aß1₋42 astrocytic activation].

This study was aimed to investigate the protective effect and mechanism of ß-asarone on PC12 cells injury induced byAß1₋42 activated astrocytes, and provide experimental basis for ß-asarone application in the prevention and control of Alzheimer's disease (AD). Firstly, RA-h and PC12 cells were co-cultured in the special transwell chamber, and the Real time cell analysis (RTCA) system was used to real-time observe its effect on PC12 cells survival rate in the co-culture system after astrocytes injury induced by Aß1₋42. The best intervention time of ß-asarone was selected according to the survival curve and parameters generated automatically. ß-asarone with different concentrations was used for intervention on astrocytes, then the changes of PC12 cells survival rate in the co-culture system were observed. Secondly, MTT assay was used to detect the effect of Aß1₋42 on PC12 cells survival rate as well as the intervention effect of ß-asarone, and verify the testing results of RTCA. The levels of IL-1ß, TNF-α and BDNF in culture media of the lower chamber were detected by ELISA. The NF-κB activity and phosphorylation levels of ERK, p38 and JNK were detected by Western blot. Results showed that ß-asarone (55.5 mg•L⁻¹) could significantly slowdown the decline of PC12 cells survival rate caused by Aß1₋42-induced RA-h activation (P<0.01), significantly reduce the levels of IL-1ß, TNF-α and the phosphorylation levels of ERK, p38 and JNK in culture media of the lower chamber (P<0.01). ß-asarone(166.7 mg•L⁻¹) could promote the release of BDNF in culture media of the lower chamber(P<0.05). These results indicated that Aß1₋42 could induce RA-h activation and its release of IL-1ß, TNF-α and other inflammatory factors to aggravate the PC12 cells injury; ß-asarone could reduce the levels of IL-1ß, TNF-α, promote the release of BDNF, and inhibit the NF-κB activity as well as phosphorylation levels of ERK, p38 and JNK protein in PC12 cells.