A2AR activation after traumatic brain injury in the role of excessive tau protein phosphorylation and mechanism research
10.3969/j.issn.1005-1678.2017.07.008
- VernacularTitle:A2AR活化在脑创伤后tau蛋白过度磷酸化中的作用与机制研究
- Author:
Dongchun WANG
;
Xiaoli LI
;
Kun ZHANG
;
Lijuan QIN
- Keywords:
taumatic brain injury;
adenosine A2A receptor;
tau protein;
phosphorylation level;
mice were experimentally
- From:
Chinese Journal of Biochemical Pharmaceutics
2017;37(7):25-28
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the A2AR activation after traumatic brain injury mechanisms and the role of excessive tau protein phosphorylation.Methods With no specific mice experiment research of specific pathogens, position in the left parietal cortex in mice, by the method of controllable cortical against brain trauma model model, 15 min after injury in mice abdominal injection of A2AR specific inhibitors ZM241385 or use A2AR knockout mice, testing the brain neuron loss and tau protein phosphorylation level;Use specific agonists CGS21680 activate the original generation of nerve cells in the hippocampus and the A2AR human neuroblastoma cells, using immunocytochemistry and immunofluorescence test tua protein phosphorylation level of change, to observe axon transport function of mitochondria.Results Immunohistochemical results accumulation of optical density analysis showed that inhibition of A2AR activation can significantly reduce after cerebral trauma Ser404 tua protein loci phosphorylation levels, reduce excessive tua protein phosphorylation with nerve pathological change;A2AR activation after tua phosphorylation of proteins at a Ser404 site level increased significantly, nerve axons per unit length processes in the mitochondria number decreased significantly, resulting in axoplasmic transport dysfunction;To activate the original generation of nerve cells in the hippocampus and after the A2AR human neuroblastoma cells, tua protein phosphorylation Ser404 locus levels increased significantly.Conclusion A2AR activation after cerebral trauma has obvious influence on tua protein phosphorylation levels, may be a function by influencing the axoplasmic transport, eventually forming cognitive dysfunction.
