Influence Of CD200 On Inhibiting The Inflammatory Response By Regulating The K_ATP Channel Of MG Cells In PD Mice

Objective: To explore the function of CD200 in regulating adenosine triphosphate-sensitive potassium channel(KATP) of microglia(MG) cells and inhibiting the activation of MG cells and the release of inflammatory factors so as to reduce the inflammatory response in the lesion area of mice with parkinson’s disease(PD).Methods: In-vivo Mitochondrial Permeability Transition Pore(MPTP) PDmice models and Mpp+-induced in-vitro MG cell PD models were selected to detect the expression changes of CD200 and its receptor CD200 R in the cerebral tissues of PD mice models by Western-blot method; to observe the different sub-genes(Kir6.1, Kir6.2, Sur1 and Sur2) of KATP channels of MG cells; to detect the activation of cerebral tissues and MG cells in PD mice models with immunohistochemical and immunocytochemical methods; to explore the internal connection between the expression changes of CD200 and the activation of MG cells; and to detect the level changes of mRNA in corresponding inflammatory factors along with the time(IFN-γ, TNF-α and IL-1β) by Real-time PCR method and the release of inflammatory factor cells along with the time in the cerebral tissues of PD mice models by Elisa method. In-vitro induced cell PD models were applied to detect the influence of CD200 on the release of adenosine triphosphate(ATP) and to observe the effects of exogenous recombinant CD200 in impacting the opening of KATP channel of MG cells, inhibiting the activation of MG cells and regulating the release of inflammatory factors so as to further understand the role CD200 played in regulating the opening of KATP channel of MG cells and the inhibition on the inflammatory response of PD. Results: MG cells expressed Kir6.1 and Sur2 without Kir6.2 and Sur1 in the cerebral tissues of normal mice. The expressions of CD200 and CD200 R were down-regulated, MG cell activation increased and the release of IFN-γ, TNF-α and IL-1β promoted in MPTP mice models. In-vitro PD models added with exgenous-recombinant CD200 could inhibit the release of ATP, improve the opening of KATP channel, inhibit the activation of MG cells and the release of inflammatory factors induced by Mpp+ and reduce the inflammatory factors in PD models. Conclusion: In PD models, CD200 can improve the opening of KATP channel, inhibit the activation of MG cells and the release of corresponding inflammatory factors and alleviate the inflammatory responses in area of substantia nigra to achieve the purpose of protecting dopaminergic neuron by inhibiting the ATP level in MG cells.