ArticleBiomedicines2021
Quinpirole-Mediated Regulation of Dopamine D2 Receptors Inhibits Glial Cell-Induced Neuroinflammation in Cortex and Striatum after Brain Injury.
Article in Biomedicines, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Article
- Sinomenine Hydrochloride Impedes Memory Impairments via Nrf2/HO-1-Mediated Inhibition of Oxidative Stress, Neuroinflammation and Apoptosis in Mice Brain.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Control of Dopamine Signal in High-Order Receptor Complex on Striatal Astrocytes.International journal of molecular sciences · 2024Article
- Innovative Insights into Traumatic Brain Injuries: Biomarkers and New Pharmacological Targets.International journal of molecular sciences · 2024Review
- Neuroprotective effects of quinpirole on lithium chloride pilocarpine-induced epilepsy in rats and its underlying mechanisms.European journal of medical research · 2024Article
- Neuroprotective effects of osmotin in Parkinson's disease-associated pathology via the AdipoR1/MAPK/AMPK/mTOR signaling pathways.Journal of biomedical science · 2023Article
- Xanthine-Dopamine Hybrid Molecules as Multitarget Drugs with Potential for the Treatment of Neurodegenerative Diseases.Biomolecules · 2023Article
- Heteromerization of Dopamine D2 and Oxytocin Receptor in Adult Striatal Astrocytes.International journal of molecular sciences · 2023Article
- Dopamine, Immunity, and Disease.Pharmacological reviews · 2023Review
- Review
- Review
- Biomarkers in Neurodegenerative Diseases.Biomedicines · 2022Article
- Activation of dopamine D2 receptors attenuates neuroinflammation and ameliorates the memory impairment induced by rapid eye movement sleep deprivation in a murine model.Frontiers in neuroscience · 2022Article
- Inhibition of PDE10A-Rescued TBI-Induced Neuroinflammation and Apoptosis through the cAMP/PKA/NLRP3 Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- 17β-Estradiol Abrogates Oxidative Stress and Neuroinflammation after Cortical Stab Wound Injury.Antioxidants (Basel, Switzerland) · 2021Article
- RETRACTED: Deciphering the Potential Neuroprotective Effects of Luteolin against AβInternational journal of molecular sciences · 2021Article
- Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain injury is a significant risk factor for chronic gliosis and neurodegenerative diseases. Currently, no treatment is available for neuroinflammation caused by the action of glial cells following brain injury. In this study, we investigated the quinpirole-mediated activation of dopamine D2 receptors (D2R) in a mouse model of traumatic brain injury (TBI). We also investigated the neuroprotective effects of quinpirole (a D2R agonist) against glial cell-induced neuroinflammation secondary to TBI in adult mice. After the brain injury, we injected quinpirole into the TBI mice at a dose of 1 mg/kg daily intraperitoneally for 7 days. Our results showed suppression of D2R expression and deregulation of downstream signaling molecules in ipsilateral cortex and striatum after TBI on day 7. Quinpirole administration regulated D2R expression and significantly reduced glial cell-induced neuroinflammation via the D2R/Akt/glycogen synthase kinase 3 beta (GSK3-β) signaling pathway after TBI. Quinpirole treatment concomitantly attenuated increase in glial cells, neuronal apoptosis, synaptic dysfunction, and regulated proteins associated with the blood-brain barrier, together with the recovery of lesion volume in the TBI mouse model. Additionally, our in vitro results confirmed that quinpirole reversed the microglial condition media complex-mediated deleterious effects and regulated D2R levels in HT22 cells. This study showed that quinpirole administration after TBI reduced secondary brain injury-induced glial cell activation and neuroinflammation via regulation of the D2R/Akt/GSK3-β signaling pathways. Our study suggests that quinpirole may be a safe therapeutic agent against TBI-induced neurodegeneration.
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