Long-term oral administration of melatonin does not improve beta-amyloid deposition, caspase 3, and SOD2 levels in 3 aluminum-treated Tg2576 mice
TRACE ELEMENTS AND ELECTROLYTES(2018)
摘要
Objective: Alzheimer's disease (AD) is characterized by the production and deposition of amyloid-beta peptide (A beta) and neurofibrillary degeneration. It has been demonstrated that aluminum (Al) may be considered as a risk factor for developing the disease, while it is well established that A beta induces oxidative stress, neurotoxicity and apoptosis. On the other hand, melatonin is a potent antioxidant whose levels are reduced in patients of AD in relation with the progression of the disease. Therefore, restoring the suitable melatonin levels could be considered a good strategy against AD. Materials and methods: The quantity of soluble and insoluble A beta (A beta 1-40 and A beta 1-42, respectively), the main pro-apoptotic caspase (caspase-3), and the anti-apoptotic SOD2 protein levels in cortex and hippocampus of Tg2576 mice were evaluated. Animals were chronically exposed to Al and melatonin from diet and drinking water, respectively. Results: The quantity of A beta 40 was higher than the quantity of A beta 42 in brain tissues. However, no significant differences between groups were found. Regarding Casp-3 and SOD2, an interaction "genotype x treatment" was found in both tissues tested, but no significant differences between groups of treatment were noted. Conclusion: The results of the present study did not corroborate the anti-amyloidogenic and anti-apoptotic properties of melatonin. Further studies are required to confirm the tendencies here observed.
更多查看译文
关键词
aluminum,melatonin,amyloid-beta,caspase-3,SOD2
AI 理解论文
溯源树
样例
生成溯源树,研究论文发展脉络