Authors: Susmita Sil Tusharkanti Ghosh Pritha Gupta Rupsa Ghosh Syed N Kabir Avishek Roy
Publish Date: 2016/09/24
Volume: 60, Issue: 4, Pages: 421-435
Abstract
The neurodegeneration in colchicine induced AD rats cAD is mediated by cox2 linked neuroinflammation The importance of ROS in the inflammatory process in cAD has not been identified which may be deciphered by blocking oxidative stress in this model by a wellknown antioxidant vitamin C Therefore the present study was designed to investigate the role of vitamin C on colchicine induced oxidative stress linked neuroinflammation mediated neurodegeneration and memory impairments along with peripheral immune responses in cAD The impairments of working and reference memory were associated with neuroinflammation and neurodegeneration in the hippocampus of cAD Administration of vitamin C 200 and 400 mg/kg BW in cAD resulted in recovery of memory impairments with prevention of neurodegeneration and neuroinflammation in the hippocampus The neuroinflammation in the hippocampus also influenced the peripheral immune responses and inflammation in the serum of cAD and all of these parameters were also recovered at 200 and 400 mg dose of vitamin C However cAD treated with 600 mg dose did not recover but resulted in increase of memory impairments neurodegeneration and neuroinflammation in hippocampus along with alteration of peripheral immune responses in comparison to cAD of the present study Therefore the present study showed that ROS played an important role in the colchicine induced neuroinflammation linked neurodegeneration and memory impairments along with alteration of peripheral immune responses It also appears from the results that vitamin C at lower doses showed antioxidant effect and at higher dose resulted in prooxidant effects in cADThis research work was supported by the University Grant Commission Major Research Project F No 42532/2013 SR dt 22nd March 2013 Debajit Bhowmick Nanoscience and Nanocentre University of Calcutta and Dr Arijit Ghosh post doc fellow in the Neurophysiology laboratory are acknowledged for their assistances in some parts of the work
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