NFB pathway on chronic MPTP model of Parkinsons disease dopamine neurons in the early expression of BclxL dual regulation.doc

 PAGE \* MERGEFORMAT 14 NFB pathway on chronic MPTP model of Parkinson’s disease dopamine neurons in the early expression of BclxL dual regulation Of: Zhangjiang Wei Li Zhiwei CYTOCHEMISTRY [Abstract] Objective To study the NF B pathway dependent expression of Bcl xL in 1-methyl 4-phenyl 1,2,3,6 tetrahydropyridine (MPTP) chronic Parkinson’s disease (PD) model of the early expression of DA neurons in the process of of NF B pathway in the pathogenesis of PD possible role. Methods Male C57BL / 6 mice were divided into control group and model group and intervention group, and each time in the last MPTP injection point counting, divided into 12 24 h, 1 and 2 w 4 subgroups (n = 5). the dynamic behavior observed in mice and Bcl xL expression in the substantia nigra and TH-positive changes in the number of neurons and NF B inhibitor PDTC on the above results. NF B pathway results in a time-dependent effects, model time in 12 ~ 24 h, Bcl xL protein and mRNA expression increased compared with the control group (P lt;0.05), while in the 1 ~ 2 w, Bcl xL expression and control than the former group decreased (P lt;0.05); at 2 w, the TH-positive cells in model group than in the control group decreased (P lt;0.05), while the intervention group compared with model group, positive cells increased (P lt;0.05). Conclusion NF B pathway in chronic dopamine neurons in PD models of early expression of Bcl xL has a dual regulatory role. [Keywords:] Parkinson’s disease; NF B pathway; DA neurons; MPTP model of chronic Parkinson’s disease (PD) is a common degenerative disease of the central nervous system, the exact etiology and pathogenesis of the not yet clear. More and more studies show that inflammation and apoptosis in the pathogenesis of PD play an important role in both the second there is a close link between, NF B pathway is a key point of contact between the two, but at home and abroad NF B pathway in the inflammatory response in the time-dependent effect of less. T