Abstract
Objective This study is aimed at studying the effect of quercetin on the Alzheimer disease cell model induced by Aβ25-35 in PC12 cells and its mechanism of action. Methods The AD cell model was established by Aβ25-35. Quercetin was used at different concentrations (0, 10, 20, 40, and 80 μmol/L). The morphology of cells was observed, and the effect on cell survival rate was detected by the MTT method. Cell proliferation was detected by the SRB method. The contents of LDH, SOD, MDA, GSH-Px, AChE, CAT, and T-AOC were detected by kits. The expression of sirtuin1/Nrf2/HO-1 was detected by RT-qPCR and Western blot. Results PC12 cells in the control group grew quickly and adhered well to the wall, most of which had extended long axons and easily grew into clusters. In the model group, cells were significantly damaged and the number of cells was significantly reduced. It was found that PC12 cells were swollen, rounded, protruding, and retracting, with reduced adherent function and floating phenomenon. Quercetin could increase the survival rate and proliferation rate of PC12 cells; reduce the levels of LDH, AChE, MDA, and HO-1 protein; and increase the levels of SOD, GSH-Px, CAT, T-AOC, sirtuin1, and Nrf2 protein. Conclusion Quercetin can increase the survival rate of PC12 injured by Aβ25-35, promote cell proliferation, and antagonize the toxicity of Aβ; it also has certain neuroprotective effects. Therefore, quercetin is expected to become a drug for the treatment of AD.
Highlights
Alzheimer’s disease (AD) is a neurodegenerative disease that accounts for 50% of dementia cases worldwide [1]
It has been shown that the deposition of Aβ25-35 has a direct toxic effect on neurons, and it can enhance the sensitivity of neurons to harmful factors such as free radicals and oxidative stress, leading to neuronal apoptosis [6]
AD is a representative neurodegenerative disease in learning and memory impairment [1], which can be divided into primary dementia, vascular dementia, and a mixture of the two
Summary
Alzheimer’s disease (AD) is a neurodegenerative disease that accounts for 50% of dementia cases worldwide [1]. The incidence of AD is increasing year by year [2] It seriously affects the quality of life. It has become one of the most serious problems in the field of geriatrics. The specific pathogenesis of AD is not clear, but studies have found that β-amyloid (Aβ) deposition, neurofibrillar tangles, and neuronal loss are the main characteristics of AD, which are closely related to the cognitive impairment of patients [3,4,5]. It has been shown that the deposition of Aβ25-35 has a direct toxic effect on neurons, and it can enhance the sensitivity of neurons to harmful factors such as free radicals and oxidative stress, leading to neuronal apoptosis [6]. The inhibition of neuronal apoptosis induced by
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