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Xiang, Caixia, Lu, Yunwei, Hao, Renjuan, Wei, Yuyan, Hu, Yingchao, Yu, Guran. (1403). Catalpol alleviates amyloid- generation and neuronal oxidative stress injury via activating the Keap1-Nrf2/ARE signaling pathway in the immortalized lymphocytes from patients with late-onset Alzheimer’s disease and SKNMC cells co-culture model. , 27(12), 1547-1557. doi: 10.22038/ijbms.2024.78543.16982
Caixia Xiang; Yunwei Lu; Renjuan Hao; Yuyan Wei; Yingchao Hu; Guran Yu. "Catalpol alleviates amyloid- generation and neuronal oxidative stress injury via activating the Keap1-Nrf2/ARE signaling pathway in the immortalized lymphocytes from patients with late-onset Alzheimer’s disease and SKNMC cells co-culture model". , 27, 12, 1403, 1547-1557. doi: 10.22038/ijbms.2024.78543.16982
Xiang, Caixia, Lu, Yunwei, Hao, Renjuan, Wei, Yuyan, Hu, Yingchao, Yu, Guran. (1403). 'Catalpol alleviates amyloid- generation and neuronal oxidative stress injury via activating the Keap1-Nrf2/ARE signaling pathway in the immortalized lymphocytes from patients with late-onset Alzheimer’s disease and SKNMC cells co-culture model', , 27(12), pp. 1547-1557. doi: 10.22038/ijbms.2024.78543.16982
Xiang, Caixia, Lu, Yunwei, Hao, Renjuan, Wei, Yuyan, Hu, Yingchao, Yu, Guran. Catalpol alleviates amyloid- generation and neuronal oxidative stress injury via activating the Keap1-Nrf2/ARE signaling pathway in the immortalized lymphocytes from patients with late-onset Alzheimer’s disease and SKNMC cells co-culture model. , 1403; 27(12): 1547-1557. doi: 10.22038/ijbms.2024.78543.16982

Catalpol alleviates amyloid- generation and neuronal oxidative stress injury via activating the Keap1-Nrf2/ARE signaling pathway in the immortalized lymphocytes from patients with late-onset Alzheimer’s disease and SKNMC cells co-culture model

Iranian Journal of Basic Medical Sciences
مقاله 7، دوره 27، شماره 12، اسفند 2024، صفحه 1547-1557    اصل مقاله (1.7 M)
نوع مقاله: Original Article
شناسه دیجیتال (DOI): 10.22038/ijbms.2024.78543.16982
نویسندگان
Caixia Xiang1، 2؛ Yunwei Lu1، 3؛ Renjuan Hao1؛ Yuyan Wei1؛ Yingchao Hu1؛ Guran Yu* 1
1Department of Neurology, Jiangsu Province Hospital of Chinese Medicine, the Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu Province, China
2Cent Hosp Enshi Tujia & Miao Autonomous Prefectur, 158 Wuyang Ave, Enshi 445000, Hubei, Peoples R China
3Department of Neurology, Shenzhen Traditional Chinese Medicine Hospital
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 Aβ1-42 in SKNMC cells due to its high levels of oxidative stress and resulted in neuronal oxidative stress injury through inhibiting Keap1-Nrf2/ARE signaling pathway. Treatment with catalpol and N-acetylcysteine (NAC), an antioxidant, prevented the AD LCL-induced Aβ1-42 overproduction and reduced the level of β-site amyloid precursor protein cleaving enzyme-1 (BACE1) and amyloid precursor protein (APP)-C99. 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 ML385, the Nrf2 inhibitor. Therefore, we speculate that the antioxidant and anti-apoptotic effects of catalpol are mediated by activating the Keap1-Nrf2/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.
کلیدواژه‌ها
Alzheimer’s Disease؛ Amyloid beta-Peptides؛ Apoptosis؛ Catalpol؛ Oxidative stress
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