ArticleCNS neuroscience & therapeutics2025
SPP1/OPN Alleviates Post-Intracerebral Hemorrhage Depression and Cognitive Impairment via Nrf2/BDNF Signaling Activation in Mice.
Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Osteopontin in the Central Nervous System: Roles in Development, Injury, Neurodegeneration, and Neuro-Oncology.Biomolecules · 2026Review
- ECM remodeling in the mPFC exacerbates cocaine-induced hyperactivity and impairs threat vigilance.Translational psychiatry · 2026Article
- The Bone-Brain Axis: Novel Insights into the Bidirectional Crosstalk in Depression and Osteoporosis.Biomolecules · 2026Review
- GLP-1 Receptor Agonists in Neurological Disorders: From Mechanisms to Clinical Translation.Drug design, development and therapy · 2026Review
- SPP1/OPN Alleviates Post-Intracerebral Hemorrhage Depression and Cognitive Impairment via Nrf2/BDNF Signaling Activation in Mice.CNS neuroscience & therapeutics · 2025Article
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Authors and funding
7 authors.
Funding
Abstract
backgroundPost-stroke depression represents a prevalent neuropsychiatric complication following intracerebral hemorrhage (ICH), yet its underlying mechanisms remain less understood compared to ischemic stroke.
methodsThis translational investigation employed a multi-omics approach, combining bioinformatics analysis of depression-related (GSE214921) and ICH-related (GSE18193) datasets from the GEO database with experimental validation. Using a collagenase-induced striatal ICH murine model, we evaluated the effects of intranasal administration of osteopontin (OPN, encoded by SPP1) through neurobehavioral tests, histopathological evaluation, and molecular biology techniques.
resultsIntegrated bioinformatics analysis identified the SPP1 signaling pathway as a potential key regulator in post-ICH depression pathogenesis. In vivo, OPN treatment produced sustained neurobehavioral improvements at 28 days post-ICH, significantly ameliorating neurological deficits, mitigating anxiety-depressive behaviors, and enhancing spatial learning-memory performance. Histopathological evaluation revealed OPN's multifaceted neuroprotective effects, including attenuated hippocampal neuroinflammation, preserved Nissl body integrity, and restored dendritic arborization complexity. Mechanistically, OPN exerted its therapeutic effects through activation of the Nrf2/BDNF signaling axis, as pharmacological inhibition of Nrf2 with ML385 completely abrogated both neuroprotection and BDNF upregulation.
conclusionOur study is the first to demonstrate the critical role of SPP1 signaling in post-ICH depression through modulation of the Nrf2/BDNF pathway, providing novel therapeutic targets for clinical management of this debilitating neuropsychiatric sequela.
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