Molecular chaperone α-crystallin prevents detrimental effects of neuroinflammation

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Silver nitrate administration stimulates immune activation, inflammation and deterioration in cell function. It is well established that hippocampal and cortical tissue are susceptible to degeneration in responses to insult such as oxidative stress or infection. This study was designed to investigate the prophylactic effect of α-crystallin, a major chaperone lens protein comprising of α-A and α-B subunits in inflammation induced mice. Mice were divided into three groups (n = 6 in each), control, inflammation and α-crystallin treated. Our result shows that α-crystallin pretreatment effectively diminished systemic inflammation induced glial fibrillary acidic protein (GFAP) and nuclear factor kappa B (NFκB) expression in the mice neocortex, reversed elevated intracellular calcium levels, acetylcholine esterase activity and depletion of glucose. Furthermore it also significantly prevented nitric oxide (P < 0.05) and lipid peroxide production in the plasma, liver, neocortex and hippocampus of the inflammation-induced mice. In order to demonstrate the direct •OH and nitric oxide radical scavenging ability of α-crystallin, an In vitro experiment using primary astrocyte culture subjected to lipopolysaccharide (LPS), a well-known inflammatory stimuli were also carried out. This study reiterates that α-crystallin therapy may serve as a potent pharmacological agent in neuroinflammation. © 2005 Elsevier B.V. All rights reserved.




Masilamoni, J. G., Jesudason, E. P., Baben, B., Jebaraj, C. E., Dhandayuthapani, S., & Jayakumar, R. (2006). Molecular chaperone α-crystallin prevents detrimental effects of neuroinflammation. Biochimica et Biophysica Acta - Molecular Basis of Disease, 1762(3), 284–293.

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