2002Unpublished venueRequires access

Effect of Beta-amyloid Peptide on NO/NOS and Free Radicals Content in Rat Model of Alzheimer Disease

Miao Jian

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Abstract

Objective To investigate whether NO, NOS and free radicals take part in the whole processing formation of Alzheimer disease(AD).Methods The AD rat model was established by injection of beta amyloid peptide(Aβ1 40,10 μg) into cerebral ventricular system. NO, NOS, CAT, T AOC,and ChE levels with consecutive changes(1,2, 3 week after injection) in brain tissue were tested.Results ChE,CAT and T AOC levels in brain were significantly decreased after 1 week Aβ infusion,NoandNOSconcentrationswereremarkedly increased than that of control group(P 0 01).ChE,CAT and T AOC levels in brain tissue were significantly decreased at 2 and 3 week than that of control group.However ,no changes of NO and NOS levels at 2 and 3 week than that at 1 week were observed.There was a positive relationship between rat memory peformence and changes of indicators.Conclusions Aβ could evoke oxidative stress,that decreased anti oxidative function to decrease.The increased NO and NOS levels in brain tissue were related closely to memory impairment, which indicated oxidative stress and NO/NOS induced by Aβ played the role in AD formation process. It mihgt be one of the mechanisms of Aβ neurotoxicity in AD.

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Objective To investigate whether NO, NOS and free radicals take part in the whole processing formation of Alzheimer disease(AD).Methods The AD rat model was established by injection of beta amyloid peptide(Aβ1 40,10 μg) into cerebral ventricular system. NO, NOS, CAT, T AOC,and ChE levels with consecutive changes(1,2, 3 week after injection) in brain tissue were tested.Results ChE,CAT and T AOC levels in brain were significantly decreased after 1 week Aβ infusion,NoandNOSconcentrationswereremarkedly increased than that of control group(P 0 01).ChE,CAT and T AOC levels in brain tissue were significantly decreased at 2 and 3 week than that of control group.However ,no changes of NO and NOS levels at 2 and 3 week than that at 1 week were observed.There was a positive relationship between rat memory peformence and changes of indicators.Conclusions Aβ could evoke oxidative stress,that decreased anti oxidative function to decrease.The increased NO and NOS levels in brain tissue were related closely to memory impairment, which indicated oxidative stress and NO/NOS induced by Aβ played the role in AD formation process. It mihgt be one of the mechanisms of Aβ neurotoxicity in AD.

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Available abstract

Objective To investigate whether NO, NOS and free radicals take part in the whole processing formation of Alzheimer disease(AD).Methods The AD rat model was established by injection of beta amyloid peptide(Aβ1 40,10 μg) into cerebral ventricular system. NO, NOS, CAT, T AOC,and ChE levels with consecutive changes(1,2, 3 week after injection) in brain tissue were tested.Results ChE,CAT and T AOC levels in brain were significantly decreased after 1 week Aβ infusion,NoandNOSconcentrationswereremarkedly increased than that of control group(P 0 01).ChE,CAT and T AOC levels in brain tissue were significantly decreased at 2 and 3 week than that of control group.However ,no changes of NO and NOS levels at 2 and 3 week than that at 1 week were observed.There was a positive relationship between rat memory peformence and changes of indicators.Conclusions Aβ could evoke oxidative stress,that decreased anti oxidative function to decrease.The increased NO and NOS levels in brain tissue were related closely to memory impairment, which indicated oxidative stress and NO/NOS induced by Aβ played the role in AD formation process. It mihgt be one of the mechanisms of Aβ neurotoxicity in AD.

Key concepts: Oxidative stress, Neurotoxicity, Endocrinology, Internal medicine, Brain tissue, Amyloid (mycology), BETA (programming language), Amyloid beta

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