Serotonin Sensitivity and Withdrawal With Low-Dose Venlafaxine

Khan, Shehryar; Sivananthan, Mauran; Bacon, Opal

doi:10.4088/pcc.18l02334

Cited by 2 publications

(1 citation statement)

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“…Venlafaxine is a dual antidepressant for serotonin and norepinephrine reuptake inhibitors. [19][20][21][22] Venlafaxine can selectively block the 5-hydroxytryptamine transporter and norepinephrine transporter, and it has a very low affinity for cholinergic, histaminergic, and adrenergic receptors. 23 Its pharmacological properties are unique with no obvious adverse reactions caused by tricyclic antidepressants.…”

Section: Introductionmentioning

confidence: 99%

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

Geng¹,

Li²,

Wang³

et al. 2021

NDT

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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.

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