ArticleNeuropsychiatric disease and treatment2021
Venlafaxine Inhibits the Apoptosis of SHSY-5Y Cells Through Active Wnt/β-Catenin Signaling Pathway.
Article in Neuropsychiatric disease and treatment, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 5 citations in OpenAlex.
- Computational biological analysis reveals that HIF-1 and FoxO signaling pathways influence cognitive impairment in patients with depression.Translational psychiatry · 2025Article
- Extracellular vesicles from water kefir can interact with human neurons in vitro: a potential explanation for the role of probiotics consumption in mental health.AIMS neuroscience · 2025Article
- MiR-181a-5p knockdown ameliorates sevoflurane anesthesia-induced neuron injury via regulation of the DDX3X/Wnt/β-catenin signaling axis.Experimental brain research · 2024Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study aimed to explore the mechanism of venlafaxine in regulating the apoptosis of SHSY-5Y cells induced by hypoxia.
methodsThe 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.
resultsUnder 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.
conclusionVenlafaxine regulates apoptosis induced by hypoxia through the Wnt/β-catenin signaling pathway, which provides a new theoretical basis for the treatment of depression.
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