Role of dopamine in regulating microglia inflammatory responses through TLR4-NFb pathway

Abstract

Parkinsons disease (PD) is a prevalent neurodegenerative disorder that affects a significant portion of the population. One of its distinguishing features is the gradual loss of dopaminergic cells in a specific region of the brain known as the substantia nigra. In recent years, researchers have uncovered that neuroinflammation facilitates the developmental process of PD. Specifically, studies have shown that the activation of microglia, the brains immune cells, is closely linked to the levels of dopamine secreted by neurons. However, the influence of dopamine on activated microglia in PD has not been fully explored. In this study, we aimed to explore the impact of dopamine on activated microglia. To establish an activated microglia model, we used BV-2 cell lines and treated them with lipopolysaccharide (LPS) at a concentration of 200 ng/ml. Two separate groups were then exposed to dopamine at concentrations of 2 M and 10 M, respectively, to simulate dopamine treatment in the brain. To assess the effects of dopamine, we performed real-time PCR to measure the relative mRNA levels of pro- and anti-inflammatory cytokines, conducted immunofluorescent staining to observe and analyze the cell morphology, carried out a phagocytosis assay to assess the cells phagocytic ability, and conducted western blotting to identify the specific pathway through which dopamine affects microglia activation. Our findings revealed that dopamine can modulate the activation state of microglia and reduce the cells inflammatory responses via the TLR4-NFB pathway. This suggests that dopamine has the potential to alleviate neuroinflammation in PD, opening up new avenues for future treatments and therapies.