ArticleFrontiers in immunology2026
STN-DBS exerts neuroprotection and anti-inflammatory effects in a Parkinson's disease rat model.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Parkinson's disease (PD) is a progressive neurodegeneration disease characterized by dopaminergic (DA) neuron loss, with chronic neuroinflammation. Subthalamic nucleus deep brain stimulation (STN-DBS) is clinically effective for the relief of parkinsonism motor symptoms. Here, we used a homemade device to investigate the effect of STN-DBS on neuroprotection and chronic neuroinflammation in a unilateral 6-hydroxydopamine (6-OHDA)-induced PD rat model. Method: Male Sprague-Dawley rats received 6-OHDA injections into the striatum, followed by ipsilateral STN electrode implantation and high-frequency stimulation. Motor function was assessed by open-field and apomorphine-induced rotation tests. DA neuron survival, glial phenotype changes, and nuclear factor (NF)-κB pathway activity in the nigrostriatal system were evaluated using Western blotting, immunofluorescence, and RT-qPCR. Results: STN-DBS improved motor deficits and decreased the loss of tyrosine hydroxylase-positive neurons. It promoted astrocytes presented a neuroprotective phenotype and increased expression of brain-derived neurotrophic factor, and microglia mainly presented an anti-inflammatory M2 phenotype instead of a pro-inflammatory M1 phenotype. These effects may be associated with IκB-α stabilization, the suppression of NF-κB hyperactivation, and the consequent reduction in the release of downstream pro-inflammatory cytokines. Conclusion: Our findings highlight that our homemade device for STN-DBS is capable of inhibiting NF-κB, modulating glial phenotypes, mitigating neuroinflammation, and ultimately ameliorating parkinsonism deficits.
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