| Objictive:To explore the affect and the damage factors of impaired CD200-CD200R-mediated microglia silencing on degeneration of midbrain dopaminergic neuronsMethod:At experiment1an anti-CD200R blocking antibody was used to deal with the mesencephalic neuron cultures with rotenone or iron, and while establishing a phosphate saline buffer control group. We detect the content of dopamine intake oxide formation and inflammatory factors such as tumor necrosis factor alpha and interleukin6.At experiment2that different age groups (95days to660days) health Sprague-Dawley (SD) rats were executed to detect CD200expression and microglial response (MHCII mRNA and ICAM-1protein) in the substantia nigra. All statistical analyses were performed using SAS software (version6.12). Values of p<0.05were considered statistically significant.Results:(1) As comparing to the control group, the intake of DA, oxide formation and the content of TNF-a and IL-6were obviously increase in ACDR treatment group, the difference was statistically significant (p<0.05).(2) As comparing to the young group, the expression of CD200significantly less and MHCII mRNA and ICAM-1expression is obviously enhanced in the elderly group, the difference was statistically significant (p<0.05).Conclusion:(1) Dopaminergic neurons neurotoxicity was induced by rotenone and iron in mesencephalic neuron cultures. Microglia were shown to mediate dopaminergic neurotoxicity induced by the combination of ACDR and Rot(or Ir), dopaminergic neurons neurotoxicity depends on the intake of dopamine, oxide formation and TNF alpha and IL-6which play a key role on the dopaminergic neurons neurotoxicity. ACDR significantly improve the dopaminergic neurons to the susceptibility of neurologic toxicity.(2) In the substantia nigra CD200expression is reduced at the same time also comes with microglia response reinforced with aging, aging is one reason of the CD200-CD200R-mediated microglia silencing impaired. |
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