Neuroprotective effects and mechanisms of the YiQiWenYangSanHan formula on Parkinson's disease mice

IF 2.9 Q3 NEUROSCIENCES
Jinling Liu , Dong Di , Suping Sun , Yan Sun , Shihan Zhou , Jing Liu , Zizhen Qin , Xinyu Yang , Xiao Wang , Zheng Xu , Boran Zhu , Haoxin Wu
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Abstract

Background

Parkinson's disease (PD) is a complex neurodegenerative disease, which is often treated with obvious side effects such as dopamine replacement therapy. Our team has validated the unique advantages of the traditional Chinese medicine formula, YiQiWenYangSanHan formula (YQWYSHF), through in vitro experiments, confirming its therapeutic potential for PD. Nevertheless, further research and validation are required to fully understand its protective effects and underlying mechanisms against PD.

Aim of this review

This study employed an in vivo model to investigate the effects of YQWYSHF on motor impairments, neuroinflammation, and mitochondrial dysfunction in C57BL/6 J mice caused by MPTP.

Materials and methods

Sixty C57BL/6 J mice were randomly divided into 5 groups, all groups except the control group were intraperitoneally administered MPTP for 7 days (30 mg/kg). After 4 weeks of drug intragastric treatment, we assessed the dyskinesia of mice treated with different doses of YQWYSHF by behavioral examination. Additionally, immunofluorescence was used to examine the expression of ionized calcium binding adaptor protein 1 (IBA1) and glial fibrillary acidic protein-positive (GFAP) cells. Western blotting was used to assess the expression level of tyrosine hydroxylase (TH), pyrin domain-containing 3 protein (NLRP3), apoptosis-associated speck-like proteins (ASC), cysteine-containing aspartate protease-1 (Caspase-1), interleukin-1β (IL-1β), α-synuclein (α-syn), poly (ADP-ribose) polymerase 1 (PARP1), and poly ADP ribose (PAR). Furthermore, transmission electron microscopy revealed mitochondrial impairment in the neuronal cells of the substantia nigra (SN).

Results

YQWYSHF treatment alleviated dyskinesia in a mouse model of PD. Moreover, it increased the TH expression, and could reverse the increase of IBA1, GFAP, NLRP3, ASC, caspase-1,IL-1β, α-syn, PARP1 and PAR proteins induced by MPTP.

Conclusions

YQWYSHF protects dopaminergic neurons in PD by attenuating neuroinflammation and mitochondrial dysfunction. This study provides new evidence for the clinical application of traditional Chinese medicine in the treatment of PD.
益气温养散寒方对帕金森病小鼠神经保护作用及机制研究
背景帕金森病(PD)是一种复杂的神经退行性疾病,其治疗往往有明显的副作用,如多巴胺替代疗法。我们的团队通过体外实验验证了中药复方益气温养散寒(YQWYSHF)的独特优势,证实了其治疗PD的潜力。然而,需要进一步的研究和验证,以充分了解其对PD的保护作用和潜在机制。本研究采用体内模型,研究YQWYSHF对MPTP引起的C57BL/6 J小鼠运动障碍、神经炎症和线粒体功能障碍的影响。材料与方法将60只C57BL/6 J小鼠随机分为5组,除对照组外,其余各组均腹腔注射MPTP(30 mg/kg) 7 d。灌胃给药4周后,我们通过行为学检查来评估不同剂量的青芪芪对小鼠运动障碍的影响。此外,免疫荧光检测离子钙结合接头蛋白1 (IBA1)和胶质纤维酸性蛋白阳性(GFAP)细胞的表达。Western blotting检测酪氨酸羟化酶(TH)、含pyrin结构域3蛋白(NLRP3)、凋亡相关斑点样蛋白(ASC)、含半胱氨酸天冬氨酸蛋白酶-1 (Caspase-1)、白介素-1β (IL-1β)、α-突触核蛋白(α-syn)、聚(ADP-核糖)聚合酶1 (PARP1)、聚ADP核糖(PAR)的表达水平。透射电镜显示黑质(SN)神经元细胞线粒体损伤。结果syqwyshf治疗可减轻PD模型小鼠运动障碍。此外,它能提高TH的表达,并能逆转MPTP诱导的IBA1、GFAP、NLRP3、ASC、caspase-1、IL-1β、α-syn、PARP1和PAR蛋白的升高。结论syqwyshf通过减轻神经炎症和线粒体功能障碍,保护PD患者多巴胺能神经元。本研究为临床应用中药治疗帕金森病提供了新的依据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
IBRO Neuroscience Reports
IBRO Neuroscience Reports Neuroscience-Neuroscience (all)
CiteScore
2.80
自引率
0.00%
发文量
99
审稿时长
14 weeks
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