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Abstract

Investigation of the Mechanism of silencing microRNA-665 Expression in Depression via the Phosphoinositide 3-Kinase/Protein Kinase B/c-Jun N-Terminal Kinase Pathway

Author(s): Fei Gao*, Liangsong Li, Qian Hu and Dechen Wang
School of Chinese Classics, Beijing University of Chinese Medicine, Chaoyang, Beijing 100013, 1Department of Science and Education, The Fourth People’s Hospital of Liaocheng, Liaocheng, Shandong Province 252003, China

Correspondence Address:
Fei Gao, School of Chinese Classics, Beijing University of Chinese Medicine, Chaoyang, Beijing 100013, China, E-mail:18810900206@163.com


This study explores the consequences of microRNA-665 suppression on depression, shedding light on the mechanisms involved through the phosphoinositide 3-kinase/protein kinase B/c-Jun N-terminal kinase signaling pathways. The findings aim to identify new therapeutic targets and offer deeper insights for treating depression. To model depression, mice were subjected to a chronic unpredictable mild stress protocol and subsequently distributed randomly into four groups; control, depression model, microRNA-665 silencing, and microRNA-665 silencing combined with phosphoinositide 3-kinase/protein kinase B inhibitor. MicroRNA-665 expression was silenced using adenoviral vectors. Serum cortisol levels were measured using enzyme-linked immunosorbent assay. In the depression model, silencing microRNA-665 notably decreased immobility duration in both the forced swim test and the tail suspension test. Additionally, it led to a significant increase in the total movement distance observed in the open field test. Enzyme-linked immunosorbent assay results showed a decrease in serum cortisol levels in the microRNA-665 silencing group. Reverse transcription-quantitative polymerase chain reaction analysis indicated that silencing microRNA-665 regulated the expression levels of phosphoinositide 3-kinase, protein kinase B, and c-Jun N-terminal kinase genes towards normal levels. Silencing miR-665 expression significantly improved the behavioral performance of depressed mice and normalized the levels of associated proteins and genes through the phosphoinositide 3-kinase, protein kinase B, and c-Jun N-terminal kinase signaling pathways, as well as regulated physiological indicators associated with depression.

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