Neuroprotective effect and mechanism of eleutheroside B on Parkinson’s disease model mice by regulating the IKKβ/NF-κB signaling pathway
- VernacularTitle: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
- Author:
Xiaoli WANG
1
;
Hua RONG
2
;
Siwen PAN
3
;
Chunlei YU
2
;
Tianjiao XU
2
;
Yu SUN
2
;
Huan CONG
1
;
Yu PANG
4
;
Gang CHEN
5
;
Xiaoming LI
2
Author Information
1. School of Pharmacy，Qiqihar Medical University，Heilongjiang Qiqihar 161006，China
2. Institute of Medical and Pharmaceutical Sciences，Qiqihar Medical University，Heilongjiang Qiqihar 161006，China
3. College of Pathology，Qiqihar Medical University，Heilongjiang Qiqihar 161006，China
4. Dept. of the 4th Neurology，the Second Affiliated Hospital of Qiqihar Medical University，Heilongjiang Qiqihar 161000，China
5. Dept. of Scientific Research，Qiqihar Medical University，Heilongjiang Qiqihar 161006，China
- Publication Type:Journal Article
- Keywords:
eleutheroside B;
Parkinson’s disease;
behavioral ability;
neuroinflammation;
neuroprotection;
IKKβ/NF-κB signaling
- From:
China Pharmacy
2026;37(8):998-1002
- CountryChina
- Language:Chinese
-
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， α -synuclein （ α -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 （ P ＜0.05）， while the levels and mRNA expressions of IL-1β， TNF-α， 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 （ P ＜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 α -syn aggregation and neuronal loss， and further improving motor dysfunction in PD mice.
