ArticleBiological research2017
Neuron-derived CCL2 contributes to microglia activation and neurological decline in hepatic encephalopathy.
Article in Biological research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 55 citations in OpenAlex.
- Review
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- Blood-brain barrier dysfunction in hepatic encephalopathy: pathophysiology, diagnostic assessment and therapeutic perspectives.Metabolic brain disease · 2025Review
- GPX4 activator enhances neuroprotection and functional recovery in spinal cord injury.Journal of orthopaedic translation · 2025Article
- The Role of Neuroinflammation in the Pathogenesis of Hepatic Encephalopathy.Journal of immunology research · 2025Review
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- Lipocalin 2 in the Paraventricular Thalamic Nucleus Contributes to DSS-Induced Depressive-Like Behaviors.Neuroscience bulletin · 2023Article
- Anti-inflammatory strategies for hepatic encephalopathy: preclinical studies.Arquivos de neuro-psiquiatria · 2023Review
- Effects of Natural Product-Derived Compounds on Inflammatory Pain via Regulation of Microglial Activation.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Neuroblasts migration under control of reactive astrocyte-derived BDNF: a promising therapy in late neurogenesis after traumatic brain injury.Stem cell research & therapy · 2023Article
- Golexanolone, a GABACNS neuroscience & therapeutics · 2022Article
- Cutaneous burn injury induces neuroinflammation and reactive astrocyte activation in the hippocampus of aged mice.Experimental gerontology · 2022Article
- Rifaximin Improves Spatial Learning and Memory Impairment in Rats with Liver Damage-Associated Neuroinflammation.Biomedicines · 2022Article
- CCL2 Inhibition of Pro-Resolving Mediators Potentiates Neuroinflammation in Astrocytes.International journal of molecular sciences · 2022Article
- The neurogliovascular unit in hepatic encephalopathy.JHEP reports : innovation in hepatology · 2021Review
- Rifaximin Prevents T-Lymphocytes and Macrophages Infiltration in Cerebellum and Restores Motor Incoordination in Rats with Mild Liver Damage.Biomedicines · 2021Article
- Fetal inflammation induces acute immune tolerance in the neonatal rat hippocampus.Journal of neuroinflammation · 2021Article
- Dendrimer-Triamcinolone Acetonide Reduces Neuroinflammation, Pathological Angiogenesis, and Neuroretinal Dysfunction in Ischemic Retinopathy.Advanced therapeutics · 2021Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCCL2 was up-regulated in neurons and involved in microglia activation and neurological decline in mice suffering from hepatic encephalopathy (HE). However, no data exist concerning the effect of neuron-derived CCL2 on microglia activation in vitro.
methodsThe rats were pretreated with CCL2 receptor inhibitors (INCB or C021, 1 mg/kg/day i.p.) for 3 days prior to thioacetamide (TAA) administration (300 mg/kg/day i.p.) for inducing HE model. At 8 h following the last injection (and every 4 h after), the grade of encephalopathy was assessed. Blood and whole brains were collected at coma for measuring CCL2 and Iba1 expression. In vitro, primary neurons were stimulated with TNF-α, and then the medium were collected for addition to microglia cultures with or without INCB or C021 pretreatment. The effect of the medium on microglia proliferation and activation was evaluated after 24 h.
resultsCCL2 expression and microglia activation were elevated in the cerebral cortex of rats received TAA alone. CCL2 receptors inhibition improved neurological score and reduced cortical microglia activation. In vitro, TNF-α treatment induced CCL2 release by neurons. Medium from TNF-α stimulated neurons caused microglia proliferation and M1 markers expression, including iNOS, COX2, IL-6 and IL-1β, which could be suppressed by INCB or C021 pretreatment. The medium could also facilitate p65 nuclear translocation and IκBα phosphorylation, and NF-κB inhibition reduced the increased IL-6 and IL-1β expression induced by the medium.
conclusionNeuron-derived CCL2 contributed to microglia activation and neurological decline in HE. Blocking CCL2 or inhibiting microglia excessive activation may be potential strategies for HE.
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