RESUMO
This study was designed to investigate the protective effects of curcumin against colchicine-induced cognitive impairment and oxidative stress in rats. Male Wistar rats (weighing 150-200 g) received colchicine intracerebroventricularly (15 microg per rat), and cognitive dysfunctions were evaluated by the Morris water maze and the plus maze performance task and supported by biochemical tests. Central administration of colchicine caused memory deficit in both the Morris water maze and the elevated plus maze task paradigm tasks. Chronic treatment with curcumin (5-50 mg/kg, p.o.) twice daily for a period of 25 days beginning 4 days prior to colchicine injection significantly improved the colchicine-induced cognitive impairment. Biochemically, chronic administration of curcumin significantly reduced the elevated lipid peroxidation, restored the decreased reduced glutathione level and acetylcholinesterase activity, and attenuated the raised colchicine-induced elevated nitrite levels. The results of the present study indicate that curcumin has a protective role against colchicine-induced cognitive impairment and associated oxidative stress.
Assuntos
Ventrículos Cerebrais/efeitos dos fármacos , Transtornos Cognitivos/tratamento farmacológico , Colchicina/administração & dosagem , Curcumina/uso terapêutico , Estresse Oxidativo/efeitos dos fármacos , Acetilcolinesterase/análise , Animais , Comportamento Animal/efeitos dos fármacos , Encéfalo/efeitos dos fármacos , Encéfalo/enzimologia , Química Encefálica , Transtornos Cognitivos/induzido quimicamente , Curcumina/farmacologia , Glutationa/análise , Peroxidação de Lipídeos/efeitos dos fármacos , Masculino , Aprendizagem em Labirinto/efeitos dos fármacos , Memória/efeitos dos fármacos , Nitritos/análise , Ratos , Ratos WistarRESUMO
Alzheimer's disease is a complex and multifactorial neurodegenerative disease. Central administration of colchicine, a microtubule-disrupting agent, causes loss of cholinergic neurons and cognitive dysfunction that is associated with excessive free radical generation. The present study was aimed at evaluating the effects of trans-resveratrol in the prevention of colchicine-induced cognitive impairment and oxidative stress in rats. Intracerebroventricular administration of colchicine (15 microg/5 microl) induced impaired cognitive functions in both the Morris water maze task and the elevated plus-maze task. Chronic treatment with resveratrol (10 and 20 mg/kg, p.o.) for a period of 25 days, beginning 4 days prior to colchicine injection, significantly improved the colchicine-induced cognitive impairment. Intracerebroventricular colchicine injection resulted in free radical generation characterized by alterations in oxidative stress markers with a significant increase in malondialdehyde (MDA) and nitrite levels and depletion of reduced glutathione (GSH) activity in the rat brains. It also showed a significant decrease in acetylcholinesterase activity. Besides improving cognitive dysfunction, chronic administration of resveratrol significantly reduced the elevated MDA and nitrite levels and restored the depleted GSH and acetylcholinesterase activity. Results of the present study indicated that trans-resveratrol has a neuroprotective role against colchicine-induced cognitive impairment and associated oxidative stress.
