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轻度刺激强度的迷走神经刺激对帕金森病模型大鼠具有抗炎和神经保护作用。

Vagus Nerve Stimulation with Mild Stimulation Intensity Exerts Anti-Inflammatory and Neuroprotective Effects in Parkinson's Disease Model Rats.

作者信息

Kin Ittetsu, Sasaki Tatsuya, Yasuhara Takao, Kameda Masahiro, Agari Takashi, Okazaki Mihoko, Hosomoto Kakeru, Okazaki Yosuke, Yabuno Satoru, Kawauchi Satoshi, Kuwahara Ken, Morimoto Jun, Kin Kyohei, Umakoshi Michiari, Tomita Yousuke, Tajiri Naoki, Borlongan Cesario V, Date Isao

机构信息

Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences.

Department of Neurosurgery, Tokyo Metropolitan Neurological Hospital, Tokyo 183-0042, Japan.

出版信息

Biomedicines. 2021 Jul 7;9(7):789. doi: 10.3390/biomedicines9070789.

DOI:10.3390/biomedicines9070789
PMID:34356853
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8301489/
Abstract

BACKGROUND

The major surgical treatment for Parkinson's disease (PD) is deep brain stimulation (DBS), but a less invasive treatment is desired. Vagus nerve stimulation (VNS) is a relatively safe treatment without cerebral invasiveness. In this study, we developed a wireless controllable electrical stimulator to examine the efficacy of VNS on PD model rats.

METHODS

Adult female Sprague-Dawley rats underwent placement of a cuff-type electrode and stimulator on the vagus nerve. Following which, 6-hydroxydopamine (6-OHDA) was administered into the left striatum to prepare a PD model. VNS was started immediately after 6-OHDA administration and continued for 14 days. We evaluated the therapeutic effects of VNS with behavioral and immunohistochemical outcome assays under different stimulation intensity (0.1, 0.25, 0.5 and 1 mA).

RESULTS

VNS with 0.25-0.5 mA intensity remarkably improved behavioral impairment, preserved dopamine neurons, reduced inflammatory glial cells, and increased noradrenergic neurons. On the other hand, VNS with 0.1 mA and 1 mA intensity did not display significant therapeutic efficacy.

CONCLUSIONS

VNS with 0.25-0.5 mA intensity has anti-inflammatory and neuroprotective effects on PD model rats induced by 6-OHDA administration. In addition, we were able to confirm the practicality and effectiveness of the new experimental device.

摘要

背景

帕金森病（PD）的主要外科治疗方法是脑深部电刺激（DBS），但人们期望有侵入性较小的治疗方法。迷走神经刺激（VNS）是一种相对安全且无脑部侵入性的治疗方法。在本研究中，我们开发了一种无线可控电刺激器，以研究VNS对PD模型大鼠的疗效。

方法

成年雌性Sprague-Dawley大鼠在迷走神经上放置袖带式电极和刺激器。随后，将6-羟基多巴胺（6-OHDA）注入左侧纹状体以制备PD模型。在给予6-OHDA后立即开始VNS，并持续14天。我们在不同刺激强度（0.1、0.25、0.5和1 mA）下，通过行为学和免疫组织化学结果分析评估VNS的治疗效果。

结果

强度为0.25 - 0.5 mA的VNS显著改善了行为障碍，保护了多巴胺能神经元，减少了炎性胶质细胞，并增加了去甲肾上腺素能神经元。另一方面，强度为0.1 mA和1 mA的VNS未显示出显著的治疗效果。

结论

强度为0.25 - 0.5 mA的VNS对6-OHDA诱导的PD模型大鼠具有抗炎和神经保护作用。此外，我们能够证实新实验装置的实用性和有效性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3559/8301489/2bcbde244b7a/biomedicines-09-00789-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3559/8301489/935900d5f000/biomedicines-09-00789-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3559/8301489/88ae4b1cf139/biomedicines-09-00789-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3559/8301489/9a5a90738a61/biomedicines-09-00789-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3559/8301489/8f91ae6810cf/biomedicines-09-00789-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3559/8301489/f99b7680b320/biomedicines-09-00789-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3559/8301489/7f999ae10c59/biomedicines-09-00789-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3559/8301489/cd4f81724e6d/biomedicines-09-00789-g007a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3559/8301489/8571464d4cf0/biomedicines-09-00789-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3559/8301489/2bcbde244b7a/biomedicines-09-00789-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3559/8301489/935900d5f000/biomedicines-09-00789-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3559/8301489/88ae4b1cf139/biomedicines-09-00789-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3559/8301489/9a5a90738a61/biomedicines-09-00789-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3559/8301489/8f91ae6810cf/biomedicines-09-00789-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3559/8301489/f99b7680b320/biomedicines-09-00789-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3559/8301489/7f999ae10c59/biomedicines-09-00789-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3559/8301489/cd4f81724e6d/biomedicines-09-00789-g007a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3559/8301489/8571464d4cf0/biomedicines-09-00789-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3559/8301489/2bcbde244b7a/biomedicines-09-00789-g009.jpg

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