Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Venlafaxine inhibits neuronal apoptosis in a depression rat model via ERK1/ERK2 pathway

Yanbin Hou¹, Yunxin Ji¹, Zhongze Lou¹, Liemin Ruan¹, He Gao²

¹Department of Psychosomatics, Ningbo First Hospital; ²Department of Psychiatry, Ningbo Kangning Hospital, Ningbo, China.

For correspondence:- He Gao Email:

Accepted: 30 June 2021 Published: 29 July 2021

Citation: Hou Y, Ji Y, Lou Z, Ruan L, Gao H. Venlafaxine inhibits neuronal apoptosis in a depression rat model via ERK1/ERK2 pathway. Trop J Pharm Res 2021; 20(7):1373-1379 doi: 10.4314/tjpr.v20i7.8

© 2021 The authors.
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Abstract

Purpose: To investigate the effects and mechanism of action of venlafaxine on neuronal apoptosis of depressed rats.

Methods: Rats were randomly divided into normal control (NC) group, depressed rats (depression) group or venlafaxine-treatment group. Changes in body weight and sucrose preference ratio were recorded and behaviors in open field test (OFT) were observed in each group. Pathological changes in and the apoptosis rate of the cerebral neurons, and the activity of extracellular signal-regulated kinase 1 (ERK1)/ERK2 pathway were observed under a microscope.

Results: At weeks 2 and 4, the body weight and water consumption of rats in depression group dropped below those of rats in NC group. On the other hand, at week 2, the body weight and water consumption of rats in venlafaxine-treatment group were significantly higher than those of rats in depression group (p < 0.05). Besides, depression group had randomly arranged neuron cells and a thinner cell layer, while venlafaxine-treatment group had a relatively regular hippocampal neural cell arrangement and a thicker cell layer. Moreover, cell apoptosis rate was higher in depression group than in that NC group, and lower in venlafaxine-treatment group than that in depression group (p < 0.05). Finally, the protein expressions of phosphorylated (p)-ERK1 and p-ERK2 were significantly higher in depression group than those in NC group (p<0.05), and distinctly lower in venlafaxine-treatment group than those in depression group (p <0.05).

Conclusion: By suppressing the activity of ERK1/ERK2 pathway, venlafaxine relieves the symptoms of depression and repairs neuronal injuries in rats, thereby suppressing neuronal apoptosis. Thus, these findings provide a novel approach for the development of new antidepressants.

Keywords: Venlafaxine, ERK1/ERK2, Depression, Neuronal apoptosis, Hippocampus, Cerebral neurons