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DL‑3‑n‑butylphthalide reduces microglial activation in lipopolysaccharide‑induced Parkinson's disease model mice
Yuhua Chen1, Mujun Jiang1, Li Li1
1Department of Neurology, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233004, P.R. China.
Abstract:
As microglial activation is a key factor in the pathogenesis of Parkinson's disease (PD), drugs that target this process may help to prevent or delay the development of PD. The present study investigated the effects of dl‑3‑n‑butylphthalide (NBP) on microglia in a lipopolysaccharide (LPS)-induced PD mouse model. The mice were randomly divided into a blank control group, LPS control group and NBP + LPS treatment group. Mice in the treatment group were given an intragastric infusion of 120 mg/kg NBP daily for 30 days during the establishment of the PD mouse model. At 4 and 28 weeks post‑treatment, the motor behaviours of the mice in each group were observed using the rotarod test and the open field test. In addition, immunohistochemical staining was performed to determine the levels of activated microglia, tumour necrosis factor‑α and α‑synuclein, and the number of tyrosine hydroxylase (TH)‑positive cells in the substantia nigra. NBP significantly improved dyskinesia, reduced microglial activation, decreased nuclear α‑synuclein deposition and increased the survival of TH‑positive cells in the substantia nigra of LPS‑induced PD model mice. These findings suggested that NBP may exert its therapeutic effect by reducing microglial activation in a mouse model of PD.
Insights
dl‑3‑n‑butylphthalide (NBP) treatment improved motor function and reduced microglial activation in a Parkinson's disease (PD) mouse model. NBP therapy protected dopamine neurons and decreased toxic protein aggregation, suggesting a therapeutic potential for PD.
Area of Science:
- Neuroscience
- Pharmacology
- Immunology
Background:
- Microglial activation is central to Parkinson's disease (PD) pathogenesis.
- Targeting microglial activation may offer a therapeutic strategy for PD.
- Lipopolysaccharide (LPS) is used to induce a PD mouse model.
Purpose of the Study:
- To investigate the effects of dl‑3‑n‑butylphthalide (NBP) on microglia in an LPS-induced PD mouse model.
- To evaluate NBP's impact on motor behavior, microglial activation, and dopaminergic neuron survival.
Main Methods:
- Mice were divided into control, LPS-induced PD, and NBP + LPS groups.
- NBP was administered intragastrically daily for 30 days.
- Motor behavior was assessed using rotarod and open field tests.
- Immunohistochemistry was used to analyze microglial activation, inflammatory markers, α‑synuclein, and tyrosine hydroxylase (TH)-positive cells.
Main Results:
- NBP treatment significantly improved motor deficits in the PD mice.
- NBP reduced microglial activation and decreased tumor necrosis factor-α levels.
- NBP decreased α‑synuclein deposition and increased the survival of TH-positive neurons in the substantia nigra.
Conclusions:
- dl‑3‑n‑butylphthalide (NBP) demonstrates therapeutic potential for Parkinson's disease.
- NBP exerts its effects by mitigating neuroinflammation, specifically reducing microglial activation.
- NBP may protect dopaminergic neurons and reduce protein aggregation in PD models.