Neuroprotective effect and mechanism of eleutheroside B on Parkinson’s disease model mice by regulating the IKKβ/NF-κB signaling pathway

WANG Xiaoli; RONG Hua; PAN Siwen; YU Chunlei; XU Tianjiao; SUN Yu; CONG Huan; PANG Yu; CHEN Gang; LI Xiaoming

doi:10.6039/j.issn.1001-0408.2026.08.05

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Neuroprotective effect and mechanism of eleutheroside B on Parkinson’s disease model mice by regulating the IKKβ/NF-κB signaling pathway

更新时间：2026-04-24

- Neuroprotective effect and mechanism of eleutheroside B on Parkinson’s disease model mice by regulating the IKKβ/NF-κB signaling pathway
- ZHONGGUO YAOFANG Vol. 37, Issue 8, Pages: 998-1002(2026)
- 作者机构：
  
  1.齐齐哈尔医学院药学院，黑龙江齐齐哈尔　161006
  2.齐齐哈尔医学院医药科学研究院，黑龙江齐齐哈尔　161006
  3.齐齐哈尔医学院病理学院，黑龙江齐齐哈尔　161006
  4.齐齐哈尔医学院附属第二医院神经内四科，黑龙江齐齐哈尔　161000
  5.齐齐哈尔医学院科研处，黑龙江齐齐哈尔　161006
- 作者简介：
- 基金信息：
- DOI：10.6039/j.issn.1001-0408.2026.08.05
  CLC： R743.3
- Received：18 December 2025，
  
  Revised：2026-03-24，
  
  Accepted：10 April 2026，
  
  Published：30 April 2026
- 稿件说明：
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王晓丽,荣华,潘思文,等.刺五加苷B调控IKKβ/NF-κB信号通路对帕金森病模型小鼠的神经保护作用及机制 [J].中国药房,2026,37(08):998-1002.

WANG Xiaoli,RONG Hua,PAN Siwen,et al.Neuroprotective effect and mechanism of eleutheroside B on Parkinson’s disease model mice by regulating the IKKβ/NF-κB signaling pathway[J].ZHONGGUO YAOFANG,2026,37(08):998-1002.
王晓丽,荣华,潘思文,等.刺五加苷B调控IKKβ/NF-κB信号通路对帕金森病模型小鼠的神经保护作用及机制 [J].中国药房,2026,37(08):998-1002. DOI： 10.6039/j.issn.1001-0408.2026.08.05.

WANG Xiaoli,RONG Hua,PAN Siwen,et al.Neuroprotective effect and mechanism of eleutheroside B on Parkinson’s disease model mice by regulating the IKKβ/NF-κB signaling pathway[J].ZHONGGUO YAOFANG,2026,37(08):998-1002. DOI： 10.6039/j.issn.1001-0408.2026.08.05.

摘要

目的

探讨刺五加苷B（ELB）调控IκB激酶β（IKKβ）/核因子κB（NF-κB）信号通路对帕金森病（PD）模型小鼠的神经保护作用及机制。

方法

将50只小鼠随机分为正常对照组、模型组、阳性对照（盐酸司来吉兰，10 mg/kg）组和ELB低、高剂量组（80、160 mg/kg），每组10只。各组小鼠灌胃相应药物或生理盐水，连续14 d；从第10天起，模型组和各给药组小鼠腹腔注射1-甲基-4-苯基-1，2，3，6-四氢吡啶30 mg/kg，连续5 d，诱导慢性PD模型。末次给药24 h后，每组随机选取6只小鼠，测试行为能力（以转棒停留时间和攀爬评分计）；检测脑组织中白细胞介素1β（IL-1β）、IL-10、肿瘤坏死因子α（TNF-α）水平及其mRNA表达，酪氨酸羟化酶（TH）阳性表达，TH、

-突触核蛋白（

-syn）、离子钙结合衔接分子1（Iba-1）蛋白表达和IKKβ、NF-κB p65蛋白磷酸化水平；观察脑黑质组织中神经元超微结构。

结果

与模型组比较，各给药组小鼠转棒停留时间和攀爬评分（ELB低剂量组除外）均显著增加（

＜0.05）；脑组织中IL-1β、TNF-α水平和其mRNA表达（ELB低剂量组TNF-α除外）以及

-syn、Iba-1蛋白表达和IKKβ、NF-κB p65蛋白的磷酸化水平均显著降低/下调，IL-10水平（ELB低剂量组除外）及其mRNA表达、TH阳性表达和蛋白表达均显著升高/上调（

＜0.05）；神经元核固缩、线粒体肿胀空泡、内质网扩张等典型神经退行性病变均有不同程度改善。

结论

ELB可能通过抑制IKKβ/NF-κB信号通路激活，减轻炎症反应、减少

‑syn异常聚集及神经元丢失，进而改善PD小鼠运动功能障碍，发挥神经保护作用。

Abstract

OBJECTIVE

To investigate the neuroprotective effect and mechanism of eleutheroside B （ELB） on Parkinson’s disease （PD） model mice by regulating the IκB kinase β （IKKβ）/nuclear factor-κB （NF-κB） signaling pathway.

METHODS

Fifty mice were randomly divided into normal control group， model group， positive control group （selegiline hydrochloride， 10 mg/kg）， and ELB low-dose and high-dose groups （80， 160 mg/kg）， with 10 mice in each group. Each group was given relevant medicine or normal saline intragastrically for 14 consecutive days. Starting from the 10th day of administration， the model group and all administration groups were intraperitoneally injected with 1-methyl-4-phenyl-1，2，3，6-tetrahydropyridine （MPTP） 30 mg/kg， for five consecutive days to establish the chronic PD model.

After the last administration for 24 h， six mice were randomly selected from each group to test their behavioral abilities； detect the levels of interleukin-1β （IL-1β）， IL-10， tumor necrosis factor-α （TNF-α） in brain tissue and their mRNA expressions were measured， and positive expression of tyrosine hydroxylase （TH）， protein expressions of TH，

-synuclein （

-syn）， ionized calcium-binding adaptor molecule 1 （Iba-1）， as well as phosphorylation levels of IKKβ and NF-κB p65 proteins in the brain tissue were detected. The ultrastructure of neurons in substantia nigra was observed.

RESULTS

Compared with the model group， rotarod endurance time and climbing score of each administration group （except for the ELB low-dose group） were increased significantly （

＜0.05）， while the levels and mRNA expressions of IL-1β， TNF-α，

-syn， and Iba-1， as well as phosphorylation levels of IKKβ and NF-κB p65 proteins in brain tissue were decreased significantly （except for TNF-α in the ELB low-dose group）. Conversely， the level and mRNA expression of IL-10 （except for the ELB low-dose group）， TH positive expression and protein expressions were significantly increased （

＜0.05）. Typical neurodegenerative pathological changes， such as neuronal karyopyknosis， mitochondrial swelling and vacuolization， and endoplasmic reticulum dilation， all showed varying degrees of improvement.

CONCLUSIONS

ELB may exert neuroprotective effects by inhibiting the activation of the IKKβ/NF-κB signaling pathway， alleviating inflammatory responses， reducing abnormal

-syn aggregation and neuronal loss， and further improving motor dysfunction in PD mice.

关键词

Keywords

references

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