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文拉法辛 (Venlafaxine) 通过活跃的 Wnt/β-Catenin 信号通路抑制 SHSY-5Y 细胞凋亡
Authors Geng R, Li H, Wang H, Ye C, Mao Y, Huang X
Received 1 December 2020
Accepted for publication 1 April 2021
Published 21 April 2021 Volume 2021:17 Pages 1145—1151
DOI https://doi.org/10.2147/NDT.S294998
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 5
Editor who approved publication: Dr Yuping Ning
Objective: This study aimed to explore the mechanism of venlafaxine in regulating the apoptosis of SHSY-5Y cells induced by hypoxia.
Methods: The CoCl2-induced neuronal hypoxia model was established based on SHSY-5Y cells. The morphology and related protein expression of SHSY-5Y cells were detected by qPCR, ELISA and Western blot.
Results: Under the condition of hypoxia-induced by CoCl2, the expression of HIF-1α in SHSY-5Y cells was up-regulated and the expression of β-catenin was down-regulated. After adding siRNA targeting HIF-1 α to the culture cell system, down-regulation of β -catenin expression in SHSY-5Y cells was restored. This confirmed the existence of the “hypoxia-HIF-1α-Wnt/β-catenin-depression” axis. Further studies have shown that venlafaxine can alleviate neuronal apoptosis induced by hypoxia by upregulating the Wnt/β-catenin signaling pathway.
Conclusion: Venlafaxine regulates apoptosis induced by hypoxia through the Wnt/β-catenin signaling pathway, which provides a new theoretical basis for the treatment of depression.
Keywords: venlafaxine, Wnt/β-catenin, SHSY-5Y cells, apoptosis