Inhibitory Effect of Chitooligosaccharide on Neuronal Apoptosis Induced by Beta-amyloid_(25-35) (Aβ_(25-35)) in Rat Pheochromocytoma (pc-12) cell

Abstract

Alzheimer disease (AD) is the most common age-related neurodegenerative disorder that affects the brain, and the cause of dementia in the elderly. The major factor of AD is the beta-amyloid (Aβ), which generates reactive oxygen species (ROS) in the cell. In this research, we evaluated the inhibition of COS on the ROS-induced apoptosis generated by Aβ25-35 in the rat pheochromocytoma (pc-12) cells. Treatment of COS showed the increasing inhibitory effect on gene and protein expression levels of not only p53 and p21 but also other apoptosis-related genes such as caspases, cytochrom c, and Apaf-1. Cell cycle analysis of pc-12 cells in the presence of COS confirmed that COS reduced cell cycle arrest at S phase. These result showed that COS is effective to inhibit the formation ROS, therefore, COS can inhibit neuronal apoptosis induced by Aβ25-35 in the pc-12 cells. Moreover, there are some evidences that acetylcholinesterase (AChE) plays a key role in modulating the cytotoxicity of Aβ. This research also showed that COS can inhibit AChE activity. These results suggest that COS has potential ability as a restrainer of AD.