Chinese Journal of Cerebrovascular Diseases 2014;(11):595-598

doi:11.3969/j.issn.1672-5921.2014.11.007

Expression of proprotein convertase 1 and neuropeptide Y after focal cerebral ischemia in mice

Zhengyu LIANG ; Songshan TANG ; Peng WANG ; Guangzhong CHEN ; Yanwen LI ; Chongxian HOU ; Dong ZHOU

Keywords

Brain ischemia; Proprotein convertase 1; Neuropeptide Y; Middle cerebral arteryocclusion model; Mice

Country

China

Language

Chinese

Abstract

Objectives Tostudytheexpressionchangesofproproteinconvertase1(PC1)incerebral cortex nerve cells and its substrate neuropeptide Y (NPY)after focal cerebral ischemia in mice and to investigatetheeffectofPC1inneuronalischemicinjury.Methods Twenty-fourmaleC57micewere randomly allocated into a sham-operation group,an ischemia-reperfusion 4-or 24-hour group with computer (n=8 in each group). A rat model of middle cerebral artery occlusion was induced by the intraluminal suture method. Western blot and real-time quantitative nucleic acid amplification were used to detect the expression changes of PC1,NPY,and mRNA in mouse cortical neurons. Results (1)Compared with the sham operation group,the expression of PC1 mRNA of ischemic cortex brain tissue at ischemic side in the ischemia-reperfusion 4-hour group increased 2. 66 ± 0. 24 and in the ischemia-reperfusion 24-hour group expressed 2. 07 ± 0. 23 (all P<0. 05). Compared with the sham operation group,the PC1 precursor protein level increased significantly at 4 hours (P<0. 05). There was no significant difference in the 24-hour group (P >0. 05 ). (2 )Compared with the sham operation group,the preproNPY mRNA and protein level increased significantly after reperfusion in the ischemia-reperfusion 4-hour group (P < 0. 05 ),the mRNA expressed 2. 31 ± 0. 27,and the increase of precursor protein level continued until 24 hours. Conclusion TheexpressionofprecursorPC1increasedaftercerebralischemia-reperfusioninmice, thus affecting the processing activity of PC1 ,and resulting in NPY protein,an active substrate of PC1 accumulated with the form of precursors,which may be one of the underlying mechanisms of neuronal ischemic injury.