ArticleInternational journal of molecular sciences2023
LPS Triggers Acute Neuroinflammation and Parkinsonism Involving NLRP3 Inflammasome Pathway and Mitochondrial CI Dysfunction in the Rat.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Convergent Astrocytic Failure in Parkinson's Disease: A System-Level Model of Pathogenesis and Treatment.Molecular neurobiology · 2026Review
- C-terminal Domain of the Heavy Chain of Tetanus Toxin Ameliorate Lipopolysaccharide Induced Hemiparkinsonism in Rats.Neurotoxicity research · 2026Article
- Exploring Mechanistic Targets ofInternational journal of molecular sciences · 2026Article
- Feasibility of multimodal metabolic analysis for detecting early changes in acute neuroinflammation.Journal of neuroinflammation · 2026Article
- Microglia, Astrocytes, and Oligodendrocytes in Parkinson's Disease: Neuroinflammatory Crosstalk and Emerging Therapeutic Strategies.Biomolecules · 2026Review
- The Molecular Architecture of Neurodegeneration: An Integrative Overview of Convergent Mechanisms.NeuroSci · 2026Review
- Dorsomedial striatal neuroinflammation causes excessive goal-directed action control by disrupting astrocyte function.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Folic acid modulates the Notch1/NF-κB pathway in a rat model of lipopolysaccharide-activated hippocampal microglia.Frontiers in neuroanatomy · 2026Article
- Acute systemic endotoxin administration elevates neuroimmune markers and sickness behaviors in male and femaleBrain, behavior, & immunity - health · 2025Article
- An update on the involvement of inflammatory mediators in Parkinson's disease pathogenesis.Archives of toxicology · 2025Review
- Inhibiting NLRP3 Inflammasome Activation to Alleviate Retinal Inflammation and Protect the Optic Nerve of OPTN(E50K)Mice.Inflammation · 2025Article
- Review
- Focused ultrasound on the substantia nigra enables safe neurotensin-polyplex nanoparticle-mediated gene delivery to dopaminergic neurons intranasally and by blood circulation.Discover nano · 2024Article
- Post-COVID dysautonomias: what we know and (mainly) what we don't know.Nature reviews. Neurology · 2024Review
- Effect of Systemic Inflammation in the CNS: A Silent History of Neuronal Damage.International journal of molecular sciences · 2023Review
- The gastrointestinal tract and Parkinson's disease.Frontiers in cellular and infection microbiology · 2023Review
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14 authors.
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Abstract
Whether neuroinflammation leads to dopaminergic nigrostriatal system neurodegeneration is controversial. We addressed this issue by inducing acute neuroinflammation in the substantia nigra (SN) with a single local administration (5 µg/2 µL saline solution) of lipopolysaccharide (LPS). Neuroinflammatory variables were assessed from 48 h to 30 days after the injury by immunostaining for activated microglia (Iba-1 +), neurotoxic A1 astrocytes (C3 + and GFAP +), and active caspase-1. We also evaluated NLRP3 activation and Il-1β levels by western blot and mitochondrial complex I (CI) activity. Fever and sickness behavior was assessed for 24 h, and motor behavior deficits were followed up until day 30. On this day, we evaluated the cellular senescence marker β-galactosidase (β-Gal) in the SN and tyrosine hydroxylase (TH) in the SN and striatum. After LPS injection, Iba-1 (+), C3 (+), and S100A10 (+) cells were maximally present at 48 h and reached basal levels on day 30. NLRP3 activation occurred at 24 h and was followed by a rise of active caspase-1 (+), Il-1β, and decreased mitochondrial CI activity until 48 h. A significant loss of nigral TH (+) cells and striatal terminals was associated with motor deficits on day 30. The remaining TH (+) cells were β-Gal (+), suggesting senescent dopaminergic neurons. All the histopathological changes also appeared on the contralateral side. Our results show that unilaterally LPS-induced neuroinflammation can cause bilateral neurodegeneration of the nigrostriatal dopaminergic system and are relevant for understanding Parkinson's disease (PD) neuropathology.
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