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文拉法辛通过激活Wnt/β-连环蛋白信号通路抑制SHSY-5Y细胞凋亡。

Venlafaxine Inhibits the Apoptosis of SHSY-5Y Cells Through Active Wnt/β-Catenin Signaling Pathway.

作者信息

Geng Ruijie, Li Haibin, Wang Hao, Ye Chenyu, Mao Yemeng, Huang Xiao

机构信息

Department of Psychological Medicine, Zhongshan Hospital, Fudan University, Shanghai, People's Republic of China.

Teaching Center of Experimental Medicine, Shanghai Medical College, Fudan University, Shanghai, People's Republic of China.

出版信息

Neuropsychiatr Dis Treat. 2021 Apr 21;17:1145-1151. doi: 10.2147/NDT.S294998. eCollection 2021.

DOI:10.2147/NDT.S294998
PMID:33907406
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8071209/
Abstract

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.

摘要

目的

本研究旨在探讨文拉法辛调节缺氧诱导的SHSY-5Y细胞凋亡的机制。

方法

基于SHSY-5Y细胞建立氯化钴诱导的神经元缺氧模型。采用qPCR、ELISA和蛋白质印迹法检测SHSY-5Y细胞的形态和相关蛋白表达。

结果

在氯化钴诱导的缺氧条件下，SHSY-5Y细胞中HIF-1α表达上调，β-连环蛋白表达下调。向培养细胞体系中加入靶向HIF-1α的小干扰RNA后，SHSY-5Y细胞中β-连环蛋白表达下调的情况得以恢复。这证实了“缺氧-HIF-1α-Wnt/β-连环蛋白抑制”轴的存在。进一步研究表明，文拉法辛可通过上调Wnt/β-连环蛋白信号通路减轻缺氧诱导的神经元凋亡。

结论

文拉法辛通过Wnt/β-连环蛋白信号通路调节缺氧诱导的凋亡，为抑郁症的治疗提供了新的理论依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/760f/8071209/b7c6aec1a51a/NDT-17-1145-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/760f/8071209/165e5e0eec1b/NDT-17-1145-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/760f/8071209/596ae83f6aba/NDT-17-1145-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/760f/8071209/2afe1bfdcfe3/NDT-17-1145-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/760f/8071209/24a819f426c0/NDT-17-1145-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/760f/8071209/b7c6aec1a51a/NDT-17-1145-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/760f/8071209/165e5e0eec1b/NDT-17-1145-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/760f/8071209/596ae83f6aba/NDT-17-1145-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/760f/8071209/2afe1bfdcfe3/NDT-17-1145-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/760f/8071209/24a819f426c0/NDT-17-1145-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/760f/8071209/b7c6aec1a51a/NDT-17-1145-g0005.jpg

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