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The protective effects of melatonin from oxidative damage induced by amyloid beta-peptide 25-35 in middle-aged rats
1Institute of Clinical Pharmacology, Anhui Medical University, Hefei, China. shenyuxi@mail.hf.ah.cn
Abstract:
This work investigated the ability of melatonin to prevent oxidative damage in brain tissue induced by injection of beta-amyloid peptide 25-35 (Abeta25-35) in middle-aged rats. The Morris water maze was used to evaluate the cognitive function of the rats. Thiobarbituric acid-reactive substances and antioxidative enzymes (superoxide dismutase and glutathione peroxidase) activities were measured. It was found that injection of (Abeta25-35) (20 microg) into the rat hippocampus caused an increase in the latency (the time to find the platform), the total swimming distance to the platform, and the starting angles in (Abeta25-35)-treated rats. Furthermore, a significant rise in lipid peroxidation and decrease in antioxidative enzyme activities in brain tissue were found. Melatonin (0.1, 1, and 10 mg/kg, i.g. x 10 days) improved the spatial resolution of amnesic rats in the Morris water maze test. Meanwhile, melatonin antagonized the lipid peroxidation in both the mitochondria (P < 0.01) at the doses of 0.1, 1.0, and 10 mg/kg and in the cytoplasm at the doses of 0.1 and 1.0 mg/kg. Also in the amnesic rats, melatonin (0.1, 1.0, and 10 mg/kg. i.g. x 10 days) stimulated the antioxidative enzyme activities. The results show that melatonin effectively reduced lipid peroxidation and enhanced the antioxidative enzyme activities in Abeta(25-35)-treated rats, which may contribute to the improvement of rats' learning and memory impaired by Abeta(25-35).
Insights
Melatonin administration improved cognitive function in rats with beta-amyloid induced memory impairment. This neuroprotective effect was linked to reduced oxidative stress and enhanced antioxidant enzyme activity in brain tissue.
Area of Science:
- Neuroscience
- Biochemistry
- Pharmacology
Background:
- Alzheimer's disease is characterized by beta-amyloid peptide accumulation and oxidative stress.
- Cognitive deficits are a hallmark of Alzheimer's disease, impacting learning and memory.
- Melatonin is a hormone with known antioxidant properties.
Purpose of the Study:
- To investigate the neuroprotective effects of melatonin against beta-amyloid peptide 25-35 (Abeta25-35) induced oxidative damage in rat brain.
- To evaluate the impact of melatonin on cognitive function and oxidative stress markers in an animal model of memory impairment.
Main Methods:
- Middle-aged rats were treated with Abeta25-35 to induce cognitive deficits and oxidative stress.
- Cognitive function was assessed using the Morris water maze test.
- Lipid peroxidation and antioxidative enzyme activities (superoxide dismutase, glutathione peroxidase) were measured in brain tissue.
Main Results:
- Abeta25-35 injection impaired spatial learning and memory, increased lipid peroxidation, and decreased antioxidative enzyme activity.
- Melatonin treatment dose-dependently improved cognitive performance in the Morris water maze.
- Melatonin significantly reduced lipid peroxidation and enhanced antioxidative enzyme activities in brain mitochondria and cytoplasm.
Conclusions:
- Melatonin demonstrates significant neuroprotective effects against Abeta25-35 induced brain damage.
- Melatonin's ability to reduce oxidative stress and boost antioxidant defenses contributes to improved learning and memory.
- These findings suggest melatonin as a potential therapeutic agent for conditions involving beta-amyloid pathology and cognitive decline.