1 Department of Pathology, 2 Department of Physiology, Shanxi Medical University, Taiyuan 030001, China

Abstract 

Objective
To investigate whether JNK-caspase-dependent apoptotic pathway is involved in Aβ31-35-induced apoptosis of cultured cortical neurons.
Methods
Cultured cortical neurons were treated with Aβ31-35 (25 μmol/L) for 4 h, 8 h, 16 h and 24 h, respectively. Caspase activities were measured using a spectrophotometer. Levels of c-Jun phosphorylation (p-c-Jun) and Fas ligand (FasL) expression were assessed by immunocytochemistry method and quantified using Image-pro plus11.0 image processing and analysis software.
Results
Treatment with Aβ31-35 (25 μmol/L) for 24 h induced significant increases in the activities of caspase-3 and caspase-8 in the cortical neurons. Besides, Aβ31-35 could time-dependently enhance the expression of p-c-Jun protein. Moreover, SP600125 application (100 nmol/L) could completely abolish Aβ31-35 neurotoxicity. The increase in FasL expression was detected at 8 h, 16 h and 24 h after Aβ31-35 treatment, and SP600125 (100 nmol/L) significantly inhibited FasL expression.
Conclusion
JNK-c-Jun-FasL-caspase-dependent extrinsic apoptotic pathway plays a critical role in mediating Aβ31-35-induced apoptosis of cultured neurons.

Keywords

Aβ31-35; neurotoxicity; caspase; JNK pathway

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