Quinpirole-Mediated Regulation of Dopamine D2 Receptors Inhibits Glial Cell-Induced Neuroinflammation in Cortex and Striatum after Brain Injury

Brain injury is a significant risk factor for chronic gliosis and neurodegenerative diseases. Currently, no treatment available neuroinflammation caused by the action of glial cells following brain injury. In this study, we investigated quinpirole-mediated activation dopamine D2 receptors (D2R) in mouse model traumatic (TBI). We also neuroprotective effects quinpirole (a D2R agonist) against cell-induced secondary to TBI adult mice. After injury, injected into mice at dose 1 mg/kg daily intraperitoneally 7 days. Our results showed suppression expression deregulation downstream signaling molecules ipsilateral cortex striatum after on day 7. Quinpirole administration regulated significantly reduced via D2R/Akt/glycogen synthase kinase 3 beta (GSK3-?) pathway TBI. concomitantly attenuated increase cells, neuronal apoptosis, synaptic dysfunction, proteins associated with blood–brain barrier, together recovery lesion volume model. Additionally, our vitro confirmed that reversed microglial condition media complex-mediated deleterious levels HT22 cells. This study injury-induced cell regulation D2R/Akt/GSK3-? pathways. suggests may be safe therapeutic agent TBI-induced neurodegeneration.