Original Article

Melatonin ameliorated okadaic-acid induced Alzheimer-like lesions.

Yi-peng WANG, Xian-tao LI, Shi-jie LIU, Xin-wen ZHOU, Xiao-chuan WANG, Jian-zhi WANG

Abstract

AIM:
To explore the protective effects of melatonin (Mel) on the abnormal phosphorylation of neuronal cytoskeletal proteins.
METHODS:
We generated a neuroblastoma (SH-SY5Y) cell system in which cytoskeletal proteins are abnormally phosphorylated resulting in microtubule disruption due to the marked inhibition of protein phosphatase activities by okadaic acid (OA).
RESULTS:
OA-induced declines in cell viability and mitochondrial metabolic activity were remarkably prevented by Mel. In addition, the hyperphosphorylation/accumulation of neurofilament-(NF-) H/M subunits and the disruption of microtubules, induced by OA, were significantly inhibited by Mel.
CONCLUSION:
Our results suggest multiple protective functions of Mel against a series of pathological lesions known to culminate in AD, including abnormal phosphorylation of cytoskeletal proteins, microtubule disassembly and mitochondrion-initiated cell toxicity.
Keywords:

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