| Abstract No.: | A-C1115 |
| Country: | India |
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| Title: | NEUROPROTECTIVE EFFECT OF N-ACETYLCYSTEINE IN THE DEVELOPMENT OF DIABETIC ENCEPHALOPATHY IN STREPTOZOTOCIN-INDUCED DIABETES |
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| Authors/Affiliations: | 1 Sukhdev Kamboj*; 1 Rajat Sandhir; 1 Kanwaljit Chopra;
1 Panjab University, Chandigar, India
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| Content: | Objective: Diabetes mellitus is a metabolic disease accompanied by a variety of complications. Among them, the neurological consequences are now receiving a greater attention. Diabetic encephalopathy, characterized by impaired cognitive functions, neurochemical and structural abnormalities, involves direct neuronal damage caused by intracellular glucose. The objective of the present study was to examine whether supplementation with NAC ameliorates learning and memory deficits caused by hyperglycemia-induced oxidative stress in rat model of Type 1 diabetes. Materials and Methods: Male Wistar rats (200-250g) were rendered diabetic by a single injection of streptozotocin (50 mg/kg) intraperitoneally. Control and streptozotocin-induced diabetic rats were treated with NAC in drinking water for 8 weeks. At termination the animals were tested for cognitive deficits by elevated plus maze and were decapitated to measure acetylcholinesterase activity and parameters indicating oxidative stress like lipid peroxidation, reduced glutathione, total thiol content, antioxidant enzymes like superoxide dismutase, catalase, glutathione reductase, glutathione peroxidase and glutathione-s-transferase were evaluated in different brain regions. Results: Learning and memory functions were observed to be deficit after 8 weeks of diabetes. Acetylcholinesterase activity, a marker of cholinergic function, was decreased by 15.6% in the cerebral cortex, 20.9 % in cerebellum and 14.9% in brain stem of diabetic rats. There was 21.97%, 20.4%, 25.5% increase in lipid peroxidation in cerebral cortex, cerebellum and brain stem in diabetic rats, respectively. This was accompanied by decrease in glutathione levels and total thiol content along with the activities of superoxide dismutase, catalase and glutathione reductase in all the three brain regions of diabetic rats. However, glutathione peroxidase activity increased by 11.2%, 13.6% and 23.1% respectively in cerebral cortex, cerebellum and brain stem while the activity of glutathione-s-transferase activity decreased only in cerebral cortex (21.7%) of diabetic animals.
Conclusion: Supplementation with NAC (1.5 g/kg/day in drinking water) significantly attenuated cognitive deficits and oxidative stress in diabetic rats. The results emphasize the involvement of increased oxidative stress in cognitive impairment in diabetic animals and point towards the potential of NAC as an adjuvant therapy to conventional anti-hyperglycemic regimens for the prevention and treatment of diabetic encephalopathy. |
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