电针通过犬尿氨酸途径减轻脂多糖诱导的抑郁样行为。

Electroacupuncture attenuates LPS-induced depression-like behavior through kynurenine pathway.

作者信息

Wu Xingying, Hu Rong, Jiang Shuo, Di Zhong, Chen Yi, Shi Mengting, Chen Bowen, He Kelin, Qian Kecheng, Guo Qin, Ma Ruijie

机构信息

Key Laboratory of Acupuncture and Neurology of Zhejiang Province, Department of Neurobiology and Acupuncture Research, The Third School of Clinical Medicine (School of Rehabilitation Medicine), Zhejiang Chinese Medical University, Hangzhou, China.

Department of Acupuncture and Moxibustion, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China.

出版信息

Front Behav Neurosci. 2023 Jan 10;16:1052032. doi: 10.3389/fnbeh.2022.1052032. eCollection 2022.

DOI:10.3389/fnbeh.2022.1052032

PMID:36703718

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9871460/

Abstract

BACKGROUND

A growing body of evidence suggests that inflammation and changes in glutamate neurotransmission are two pathophysiological mechanisms underlying depression. Electroacupuncture (EA) is a common therapeutic tool for the treatment of depression. However, the potential antidepressant mechanism of EA remains obscure. The change of the kynurenine pathway (KP) is the research priority of antidepressant mechanisms. This study will investigate the role of EA on lipopolysaccharide (LPS)-induced depression-like behavior and explore its possible mechanism of action.

METHODS

Lipopolysaccharide was used to induce depression-like behavior, and EA was given at Hegu (L14) and Taichong (LR3) acupoints in C57BL/6J mice. Depression-like behaviors were measured by behavioral tests, including tail suspension test (TST), sucrose preference test (SPT), force swim test (FST), and open field test (OFT). The levels of inflammatory cytokines IL-1β, IL-6, and TNF-α, and KP enzyme IDO1 were measured by qPCR and enzyme-linked immunosorbent assay (ELISA), while high-performance liquid chromatography (HPLC) was performed to detect the content of prefrontal cortex and hippocampal as well as serum glutamate, tryptophan (TRP), kynurenic (KYN), and quinolinic acid (QA).

RESULTS

The results showed that (1) as evidenced by increased spontaneous locomotor activities, decreased immobility duration, and a stronger preference for sucrose in the sucrose preference test, EA reversed LPS-challenged depressive-like behavior. (2) EA at L14 and LR3 decreased the levels of inflammatory cytokines, inhibited IDO1, and regulated KP metabolisms, as well as lowered the concentration of glutamate. (3) EA may exert anti-depression effects by acting on the kynurenine pathway.

CONCLUSION

This study evaluated the effects of EA on depression-like behaviors induced by lipopolysaccharide (LPS) and its regulation of inflammation and the glutamatergic system. Our results suggest that EA can ameliorate depression-like behaviors, lower the level of inflammation, and reduce the release of glutamate, possibly through the regulation of the kynurenine pathway in the brain.

摘要

背景

越来越多的证据表明，炎症和谷氨酸神经传递的变化是抑郁症潜在的两种病理生理机制。电针是治疗抑郁症的一种常用治疗手段。然而，电针的潜在抗抑郁机制仍不清楚。犬尿氨酸途径（KP）的变化是抗抑郁机制研究的重点。本研究将探讨电针对脂多糖（LPS）诱导的抑郁样行为的作用，并探索其可能的作用机制。

方法

采用脂多糖诱导抑郁样行为，对C57BL/6J小鼠的合谷穴（L14）和太冲穴（LR3）进行电针治疗。通过行为测试测量抑郁样行为，包括悬尾试验（TST）、蔗糖偏好试验（SPT）、强迫游泳试验（FST）和旷场试验（OFT）。采用qPCR和酶联免疫吸附测定（ELISA）检测炎性细胞因子IL-1β、IL-6和TNF-α以及KP酶IDO1的水平，同时采用高效液相色谱（HPLC）检测前额叶皮质、海马以及血清中谷氨酸、色氨酸（TRP）、犬尿氨酸（KYN）和喹啉酸（QA）的含量。