Catalpol alleviates amyloid- generation and neuronal oxidative stress injury via activating the Keap۱-Nrf۲/ARE signaling pathway in the immortalized lymphocytes from patients with late-onset Alzheimer’s disease and SKNMC cells co-culture model
- سال انتشار: 1403
- محل انتشار: مجله علوم پایه پزشکی ایران، دوره: 27، شماره: 12
- کد COI اختصاصی: JR_IJBMS-27-12_007
- زبان مقاله: انگلیسی
- تعداد مشاهده: 102
نویسندگان
Department of Neurology, Jiangsu Province Hospital of Chinese Medicine, the Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu Province, China
Department of Neurology, Jiangsu Province Hospital of Chinese Medicine, the Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu Province, China
Department of Neurology, Jiangsu Province Hospital of Chinese Medicine, the Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu Province, China
Department of Neurology, Jiangsu Province Hospital of Chinese Medicine, the Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu Province, China
Department of Neurology, Jiangsu Province Hospital of Chinese Medicine, the Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu Province, China
Department of Neurology, Jiangsu Province Hospital of Chinese Medicine, the Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu Province, China
چکیده
Objective(s): To assess the effect of catalpol, the major bioactive constituents of Rehmannia glutinosa, on our Alzheimer’s disease (AD) in vitro model.Materials and Methods: We employed the immortalized lymphocytes (lymphoblastoid cell line, LCL) from late-onset AD patients and co-cultured “them” to mimic the pathological process of late-onset AD and investigated the effect of catalpol on our AD in vitro model.Results: In the co-culture model, AD-derived LCL triggered excessive Aβ۱-۴۲ in SKNMC cells due to its high levels of oxidative stress and resulted in neuronal oxidative stress injury through inhibiting Keap۱-Nrf۲/ARE signaling pathway. Treatment with catalpol and N-acetylcysteine (NAC), an antioxidant, prevented the AD LCL-induced Aβ۱-۴۲ overproduction and reduced the level of β-site amyloid precursor protein cleaving enzyme-۱ (BACE۱) and amyloid precursor protein (APP)-C۹۹. Catalpol and NAC also enhanced the antioxidant capacity and reduced apoptosis in SKNMC cells co-cultured with AD LCL. The anti-oxidative effect of catalpol was antagonized by ML۳۸۵, the Nrf۲ inhibitor. Therefore, we speculate that the antioxidant and anti-apoptotic effects of catalpol are mediated by activating the Keap۱-Nrf۲/ARE signaling pathway.Conclusion: Catalpol affects the anti-Aβ generation and the antioxidative and antiapoptotic properties in the AD co-cultured model. So, it might be a novel natural drug and offer a potential therapeutic approach for AD.کلیدواژه ها
Alzheimer’s disease, Amyloid beta-Peptides, Apoptosis, Catalpol, Oxidative stressاطلاعات بیشتر در مورد COI
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