JNK pathway on subacute MPTP mouse model of Parkinsons disease substantia nigra COX2 expression in.docVIP

 PAGE \* MERGEFORMAT 2 JNK pathway on subacute MPTP mouse model of Parkinson’s disease substantia nigra COX2 expression in Authors: WANG Yong-sheng WEI Zi-Feng Zhang Zuo-Feng ZHOU Hong-xia ZHANG Yu-xin [Abstract] Objective: To study the JNK in the 1  methyl  4  phenyl  1,2,3,6  tetrahydropyridine (MPTP)-induced Parkinson’s disease (PD) model to the COX- 2 (COX  2) expression and regulation role, to explore the PD substantia nigra may lead to dopamine (DA) neuron degeneration inactivation mechanism. Methods: Preparation of sub-acute MPTP mouse model of PD was observed behavioral changes in mice models to observe the PD model mouse nigral tyrosine hydroxylase (TH), COX  2, phosphorylation of c  Jun expression changes; observed for JNK pathway inhibitor SP600125 on the above change. Results: mice compared with the control group, model group mice typical PD symptoms, the 3rd in the MPTP injection 6 h, substantia nigra COX  2-positive cells increased significantly, p  c  Jun-specific expression in the substantia nigra nucleus Within the first five in the MPTP after the second injection 7 d, substantia nigra TH-positive neurons in a significant loss of 65% (P