Immunomodulatory Effects of Platelet-Rich Plasma (PRP) on Neuroinflammation: Insights from B92 Glial Cells Stimulated with Heat-Killed Escherichia coli

Platelets increasingly appear to influence inflammation, including neuroinflammation. This study examines how platelet-rich plasma (PRP) modulates BV2 glial cell immune responses in sterile and infectious inflammation to assess potential neuroprotective effects. B92 glial cells were treated with PRP (0%, 5%, 10%, 20%) to model sterile inflammation. Infectious inflammation was simulated using heat-killed E. coli (1:100) combined with PRP. Cells were cultured in DMEM (low-glucose) with 10% FBS at 37°C, 5% CO₂, and 95% humidity for 24 h. Morphology, viability (MTT), phagocytosis (neutral red), oxidative stress (NBT), and expression of cytokines (TNF-α, IL-10, IL-1β) and apoptosis markers (BAX, Caspase-3, BCL-2) were assessed by qRT-PCR.PRP significantly enhanced glial cell viability and proliferation in a dose-dependent manner. The expression of the anti-apoptotic gene BCL-2 increased, whereas Caspase3 and BAX levels decreased following PRP treatment. PRP modulated cytokine profiles by reducing TNF-α expression and upregulating IL-10 in a dose-independent manner, accompanied by an increase in IL-1β expression across all concentrations. Morphological and metabolic analyses revealed that PRP mitigated inflammatory damage and preserved glial integrity, particularly under sterile inflammatory conditions. Under infectious stimulation, PRP attenuated E. coli -induced oxidative stress and preserved glial function without impairing phagocytic activity, suggesting a coordinated immunoregulatory effect. In conclusion, PRP may help control brain inflammation from injury or infection by protecting brain cells, balancing immune responses, and reducing stress. This suggests PRP could be a treatment for brain disorders.