NDLI: Nicotine Reduces the Cytotoxic Effect of Glycated Proteins on Microglial Cells

Content Provider	Springer Nature Link
Author	Khazaei, Mohammad R. Bakhti, Mostafa Habibi Rezaei, Mehran
Copyright Year	2009
Abstract	Protein glycation has been implicated to play an important role in the pathogenesis of Alzheimer’s disease and other neurological disorders. Glycation induces extensive change in the structure of proteins and leads to the formation of cross β-structures which are detected by the receptor of AGE. Activation of these receptors by glycated proteins transduces the signaling pathways which contribute to neuronal malfunctions and death. Glycated proteins can induce activation of microglia, which exacerbate the pathology of Alzheimer’s disease by causing chronic inflammation. Compounds which can decelerate glycation or prevent the structural change of proteins during glycation should be of therapeutic interest. In this study the effect of nicotine on protein glycation and structural alterations of the glycated protein were investigated. Bovine serum albumin, as a model protein, was glycated by glucose in the presence or absence of nicotine and structural changes in the protein together with the effect of glycated proteins on the activation of microglia via receptor of AGE were studied. Nicotine not only could not prevent glycation, but even increased protein glycation. However, proteins glycated in the presence of nicotine did not form β-structures. In the absence of this secondary structure glycated proteins cannot bind to the receptor of AGE on microglia. Here we showed that glycated proteins prepared in the presence of nicotine could not activate microglial cells.
Starting Page	548
Ending Page	558
Page Count	11
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	35
Issue Number	4
e-ISSN	15736903
Language	English
Publisher	Springer US
Publisher Date	2009-11-28
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Glycation Nicotine structure Microglial cells Alzheimer’s disease Neurology Biochemistry Neurosciences
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

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