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Published on: May 22, 2018
[Study on beta-amyloid peptide 1-42 induced chemokine RANTES in U251 cell]
Jie Hao1, Zhao-Dan Wang, Yun-Xia Yang
1Department of Pharmacology, West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu 610041, China.
Objective:
To study the molecular mechanisms of beta-amyloid 1-42 (Abeta1.42) induced the inflammatory response in U251 cells.
Methods:
U251 cells were treated with different concentration of Abeta1-42 (0.2-4.0 micromol/L) for 24 h, and the cell survival rate was evaluated by MTT. After treated with 2.0 micromol/L Abeta1-42 for 12, 24, 36, 48 hours, the nitric oxide content of U251 cells were detected with nitrate reductase method. The RANTES expression was tested by dual-antibody sandwich ELISA method. The expression of NF-kappaB and STAT1 were detected by the immunocytochemical staining.
Results:
Abeta1-42 decreased the survival rate of U251 cells in dose-dependent manner. The NO generated in 2 micromol/L Abeta1-42 treated U251 cells reached its peak at 24 h and gradually decreased thereafter. The expression of RANTES increased 4-fold (P < 0.01). The NF-kappaB P65, the STAT1 moved from the cytoplasm to the nucleus and expressed significantly were also observed in the 2 micromol/L Abeta1-42 treated U251 cells.
Conclusion:
Abeta1-42 decreases the survival rate of U251 cells and induce the releasing of NO and RANTES. This indicates that Abeta1-42 induced chemokine RANTES in U251 cell may be close related to the activation of NF-kappa B and STAT1.
