Affiliations: [a] Department of Pharmacy, Yantai Affiliated Hospital of Binzhou Medical University, Yantai, Shandong, China
| [b] Department of Geriatrics, Yantai Affiliated Hospital of Binzhou Medical University, Yantai, Shandong, China
| [c] Department of Rehabilitation, The People’s Hospital of Qingdao Shinan District, Qingdao, Shandong, China
| [d] Department of Neurology, Yantai Affiliated Hospital of Binzhou Medical University, Yantai, Shandong, China
Correspondence:
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Correspondence to: Weiwei Li, Department of Neurology, Yantai Affiliated Hospital of Binzhou Medical University, No. 717, Jinbu Street, MuPing District, Yantai City, 264100, Yantai, Shandong, China. Tel.: +86 13853597961; E-mail: [email protected].
Note: [1] These authors contributed equally to this work.
Abstract: Background:Long noncoding RNAs have been proven to play an important role in the progression of Alzheimer’s disease (AD). However, the function of small nucleolar RNA host gene 1 (SNHG1) in AD progression remains to be studied. Objective:To explore the role of SNHG1 in AD progression and clarify its potential mechanism. Methods:Amyloid β-protein (Aβ) was used to construct an AD cell model in vitro. The expression levels of SNHG1 and miR-361-3p were determined by quantitative real-time polymerase chain reaction. Cell viability and apoptosis were measured by cell counting kit 8 assay and flow cytometry. The levels of apoptosis-related proteins and zinc finger gene 217 (ZNF217) protein were evaluated by western blot analysis. Additionally, the contents of inflammatory cytokines and oxidative stress markers were tested by enzyme-linked immunosorbent assay. Furthermore, dual-luciferase reporter and RNA immunoprecipitation assays were used to verify the interaction between miR-361-3p and SNHG1 or ZNF217. Results:Aβ could induce cell injury, while resveratrol could reverse this effect. SNHG1 expression was positively regulated by Aβ and negatively regulated by resveratrol. SNHG1 knockdown could reverse the promotion effect of Aβ on cell injury. Moreover, SNHG1 sponged miR-361-3p, and miR-361-3p targeted ZNF217. Additionally, miR-361-3p overexpression reversed the promotion effect of SNHG1 overexpression on cell injury, and ZNF217 silencing also reversed the promotion effect of miR-361-3p inhibitor on cell injury. Conclusion:SNHG1 promoted cell injury by regulating the miR-361-3p/ZNF217 axis, which might provide a theoretical basis for molecular therapy of AD.
