Protective Effect and Mechanism of Human Lipoxin A4 on N2a Cell Injury Induced by β-Amyloid Protein 25-35
- VernacularTitle:人脂氧素A4对β淀粉样蛋白所致N2a细胞损伤的保护作用及机制研究
- Author:
Qiang WU
;
Le WU
;
Zhipeng XU
;
Min CUI
;
Jie PU
;
Fang CHEN
;
Qin LIU
- Keywords:
Human lipoxin A4;
N2a cells;
β-Amyloid protein 25-35;
Multifunctional protein P62;
TNF receptor-associated factor 6
- From:
China Pharmacist
2017;20(8):1340-1344
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the protective effect of human lipoxin A4 (LXA4) on N2a cell damage induced by β-amyloid protein 25-35 (Aβ25-35) and the underlying mechanism. Methods: Aβ25-35 was used to treat N2a cells to establish Alzheimer's disease (AD) cell injury model. Meanwhile, LXA4 was added to the experimental group at different concentrations (50, 100 and 200 nmol·L-1 ). MTT assay was used to detect the activity of N2a cells. The apoptosis was detected by Hoechst 33258-PI staining, the expression of P62 and TRAF6 mRNA was detected by RT-PCR, and the expression of P62 and TRAF6 protein was detected by Western blot. Results: Compared with that of the model group, the cell survival rate of LXA4 protective group (50,100 and 200 nmol·L-1 ) increased (P <0. 01) and the apoptosis of N2a cells induced by Aβ25-35 was reduced by LXA4 (100 and 200 nmol·L-1 ) . Compared with that of the model group, the expression of P62-mRNA and protein-P62 of N2a cells treated with Aβ25-35 increased (P <0. 05 or P <0. 01) and the expression of TRAF6-mRNA and protein-TRAF6 of N2a cells treated with Aβ25-35 were reduced (P <0. 05 or P <0. 01). Conclusion: LXA4 has protective effect on N2a cell damage induced by Aβ25-35 , and its mechanism may be related to the up-regulation of P62 gene and down-regulation of TRAF6 gene.
