Abstract
Aging is a neurodegenerative disease that leads to cognitive impairment, and an increase in oxidative stress as a major cause is an important factor. It has been reported that aging-related cognitive impairment is associated with increased oxidative damage in several brain regions during aging. As a powerful antioxidant, vitamin C plays an important role in preventing oxidative stress, but due to its unstable chemical properties, it is easily oxidized and thus the activity of antioxidants is reduced. In order to overcome this easily oxidized vulnerability, we developed NXP032 (vitamin C/DNA aptamer complex) that can enhance the antioxidant efficacy of vitamin C using an aptamer. We developed NXP032 (vitamin C/DNA Aptamin C320 complex) that can enhance the antioxidant efficacy of vitamin C using an aptamer. In the present study, we evaluated the neuroprotective effects of NXP032 on aging-induced cognitive decline, oxidative stress, and neuronal damage in 17-month-old female mice. NXP032 was orally administered at 200 mg/kg of ascorbic acid and 4 mg/kg of DNA aptamer daily for eight weeks. Before the sacrifice, a cognitive behavioral test was performed. Administration of NXP032 alleviated cognitive impairment, neuronal damage, microglia activity, and oxidative stress due to aging. We found that although aging decreases the Nrf2-ARE pathway, NXP032 administration activates the Nrf2-ARE pathway to increase the expression of SOD-1 and GSTO1/2. The results suggest that the new aptamer complex NXP032 may be a therapeutic intervention to alleviate aging-induced cognitive impairment and oxidative stress.
Highlights
Publisher’s Note: MDPI stays neutralAging is known to be a major risk factor for various age-related neurodegenerative diseases including stroke, Alzheimer’s disease, and Parkinson’s disease [1,2]
We investigated the effect of a new vitamin C/DNA aptamer complex, NXP032, on aging-induced oxidative stress and cognitive impairment
Aging-induced cognitive impairment and a decrease in brain function may be the result of numerous factors, including changes in neurotransmitters, neuronal damage, and toxic substances that accumulate in the brain over time
Summary
Publisher’s Note: MDPI stays neutralAging is known to be a major risk factor for various age-related neurodegenerative diseases including stroke, Alzheimer’s disease, and Parkinson’s disease [1,2]. Oxidative stress inevitably occurs during the aging process and plays a crucial role in progressive structural and functional damage to the brain [3]. Aging is associated with the progressive loss of neurons, which likely results in cognitive impairment. Oxidative stress reduction in the brain may play an essential role in age-related cognitive impairment and neuronal damage [5]. Neurons are damaged by microglial activation and are followed by changes in neurotransmitters and the release of cytokines [6,7]. Ionizing calcium binding adapter molecule-1 (Iba-1) plays an important role in functional changes in microglia, and in many previous studies, the expression of Iba-1 is reported to be upregulated in agingassociated diseases [8]. Activated microglia are the primary source of cellular oxidative with regard to jurisdictional claims in published maps and institutional affiliations
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