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Chronic neuroinflammation is of great importance in the pathogenesis of Parkinson's disease (PD). During the process of neuroinflammation, overactivated microglia release many proinflammatory factors, which eventually induce neurodegeneration. Inhibition of excessive microglial activation is regarded as a promising strategy for PD treatment. Src is a non-receptor tyrosine kinase that is closely related to tumors. Recently, some reports indicated that Src is a central mediator in multiple signaling pathways including neuroinflammation. The aim of our study was to demonstrate the role of Src in microglial regulation and neuroinflammation. The lipopolysaccharide (LPS)-stimulated BV2 microglia model and the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)induced PD model were applied in this study. The results showed that inhibition of Src could significantly relieve microgliosis and decrease levels of inflammatory factors. Besides, inhibition of Src function reduced the loss of dopaminergic neurons and improved the motor behavior of the MPTP-treated mice. Thus, this study not only verified the critical role of Src tyrosine kinase in neuroinflammation but also further proved that interfering neuroinflammation is beneficial for PD treatment. More importantly, this study shed a light on the hypothesis that Src tyrosine kinase might be a potential therapeutic target for PD and other neuroinflammation-related diseases.

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Computer simulations of stable xenon ((S)Xe) uptake curves were used to evaluate the effect of xenon-induced flow activation on CBF calculations by xenon-enhanced computed tomography. Estimates of flow activation were based on repeated transcranial Doppler measurements of blood velocity during 4.5 minutes of (S)Xe inhalation. The synthetic curves were generated from a generalized Kety equation that included time-varying blood flow activation. In contrast to the peak 35% increase in blood flow velocity during (S)Xe inhalation, a standard analysis of the flow-varying synthetic curves revealed only minor 3% to 5% increases in calculated CBF. It is concluded that brief xenon inhalations can provide blood flow estimates that contain minimal bias from activation.