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天芪平颤颗粒促进左旋多巴诱导的异动症大鼠模型中类淋巴系统功能的恢复。

Tianqi pingchan granule promotes recovery of glymphatic system function in a rat model of l-DOPA-induced dyskinesia.

作者信息

Liu Zhihua, Yang Shuyuan, Song Lu, Zhang Yu, Wan Ying, Gan Jing, Wu Na, Liu Zhenguo

机构信息

Department of Neurology, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.

出版信息

J Tradit Complement Med. 2024 Apr 29;15(4):380-387. doi: 10.1016/j.jtcme.2024.04.010. eCollection 2025 Jul.

DOI:10.1016/j.jtcme.2024.04.010
PMID:40677540
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12266283/
Abstract

BACKGROUND AND AIM

Tianqi Pingchan Granule (TPG), as a traditional Chinese medicine, is used in the treatment of Parkinson's disease. l-DOPA-induced dyskinesia (LID) is mentioned as a debilitating motor complication in the course of Parkinson's disease. The purpose of this study is to investigate the effects of TPG on LID via the pathway of the glymphatic system.

EXPERIMENTAL PROCEDURE

A rat model of LID was used in this study. The severity of LID was assessed by behavioural tests. Three doses of TPG were administered once a day for 3 weeks to investigate the role of TPG in behavioural characteristics of LID rats. The glymphatic function was evaluated by utilizing intracisternal infusion of a fluorescenttracer. The amyloid-β levels were measured by Enzyme-linked immunosorbent assay. The expression and distribution of, and GFAP were assessed using immunofluorescence.

RESULTS AND CONCLUSION

Dose-dependent effects of TPG in the 1behavioural characteristics were observed. Cortical and striatal influx cerebral spinal fluid tracer were reduced in LID rats with impaired AQP4 polarization. Amyloid-β, AQP4, and reactive astrogliosis was upregulated in LID rats. TPG administration increased cerebral influx of fluorescent tracer, restored polarized localization and expression of AQP4, and attenuated l-DOPA-induced amyloid-β deposits and astrogliosis. This study shows for the first time that glymphatic system function is impaired in LID and TPG attenuates abnormal involuntary movements in rats with LID by protecting the glymphatic system.

SECTION

  1. Natural Products; 3. Dietary therapy supplements; 4. History, Philosophy and Social-Cultural aspects of Traditional Medicine.

TAXONOMY CLASSIFICATION BY EVISE

identify the disease condition, the experimental approach.

摘要

背景与目的

天麻平颤颗粒(TPG)作为一种中药,用于治疗帕金森病。左旋多巴诱导的异动症(LID)是帕金森病病程中一种使人衰弱的运动并发症。本研究的目的是通过脑淋巴系统途径研究TPG对LID的影响。

实验过程

本研究使用LID大鼠模型。通过行为测试评估LID的严重程度。给予三种剂量的TPG,每天一次,持续3周,以研究TPG在LID大鼠行为特征中的作用。通过脑池内注入荧光示踪剂评估脑淋巴功能。采用酶联免疫吸附测定法测量β淀粉样蛋白水平。使用免疫荧光评估水通道蛋白4(AQP4)和胶质纤维酸性蛋白(GFAP)的表达和分布。

结果与结论

观察到TPG在行为特征方面具有剂量依赖性作用。在AQP4极化受损的LID大鼠中,皮质和纹状体的脑脊液示踪剂流入减少。LID大鼠中β淀粉样蛋白、AQP4和反应性星形胶质细胞增生上调。给予TPG可增加荧光示踪剂的脑内流入,恢复AQP4的极化定位和表达,并减轻左旋多巴诱导的β淀粉样蛋白沉积和星形胶质细胞增生。本研究首次表明,LID中脑淋巴系统功能受损,TPG通过保护脑淋巴系统减轻LID大鼠的异常不自主运动。

章节

  1. 天然产物;3. 饮食治疗补充剂;4. 传统医学的历史、哲学和社会文化方面。

EVISE分类法:确定疾病状况、实验方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d49/12266283/e66a5c9ea17f/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d49/12266283/d7fa578cc6fe/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d49/12266283/2a1f4b1780c5/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d49/12266283/11d6712119d1/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d49/12266283/8b1e8f92ef5a/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d49/12266283/c8b6db4747ff/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d49/12266283/eaebc79549f8/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d49/12266283/e66a5c9ea17f/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d49/12266283/d7fa578cc6fe/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d49/12266283/2a1f4b1780c5/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d49/12266283/11d6712119d1/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d49/12266283/8b1e8f92ef5a/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d49/12266283/c8b6db4747ff/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d49/12266283/eaebc79549f8/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d49/12266283/e66a5c9ea17f/gr6.jpg

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High-intensity interval training ameliorates Alzheimer's disease-like pathology by regulating astrocyte phenotype-associated AQP4 polarization.
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