Neural Regeneration Research ›› 2013, Vol. 8 ›› Issue (27): 2573-2580.doi: 10.3969/j.issn.1673-5374.2013.27.009

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S14G-humanin restored cellular homeostasis disturbed by amyloid-beta protein

Xue Li1, 2, Wencong Zhao3, Hongqi Yang1, 2, Junhong Zhang1, 2, Jianjun Ma1, 2   

  1. 1 Department of Neurology, Henan Provincial People’s Hospital, Zhengzhou 450003, Henan Province, China

    2 Department of Neurology, People’s Hospital of Zhengzhou University, Zhengzhou 450003, Henan Province, China

    3 Department of Pharmacology, Zhengzhou Maternal and Child Health Hospital, Zhengzhou 450012, Henan Province, China
  • Received:2013-05-09 Revised:2013-08-25 Online:2013-09-25 Published:2013-09-25
  • Contact: Xue Li, Master, Associate chief physician, dr.xue.li@ gmail.com.
  • Supported by:

    This study was supported by grants from Henan Medical Technologies R&D Program in China, No. 200703023, 201203130 and Henan Key Science and Technology Project in China, No. 112102310684.

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Abstract:

Humanin is a potential therapeutic agent for Alzheimer’s disease, and its derivative, S14G-humanin, is 1 000-fold stronger in its neuroprotective effect against Alzheimer’s disease-relevant insults. Alt-hough effective, the detailed molecular mechanism through which S14G-humanin exerts its effects remains unclear. Data from this study showed that fibrillar amyloid-beta 40 disturbed cellular ho-meostasis through the cell membrane, increasing intracellular calcium, generating reactive oxygen species, and decreasing the mitochondrial membrane potential. S14G-humanin restored these re-sponses. The results suggested that S14G-humanin blocked the effects of amyloid-beta 40 on the neuronal cell membrane, and restored the disturbed cellular homeostasis, thereby exerting a neuroprotective effect on hippocampal neurons.

Key words: neural regeneration, Alzheimer’s disease, amyloid-beta protein, wild type humanin, S14G-humanin, re-active oxygen species, mitochondrial membrane potential, grants-supported paper, neurodegeneration, neuroregeneration