Nemo-like kinase reduces neuronal apoptosis in inflammatory diseases of central nervous system
10.3760/cma.j.issn.1006-7876.2010.12.016
- VernacularTitle:Nemo样激酶抑制中枢神经系统炎症过程中神经元的凋亡
- Author:
Huoyan JI
;
Huimin WANG
- Publication Type:Journal Article
- Keywords:
Central nervous system infections;
Inflammation;
Mitogen-activated protein kinases;
PC12 cells;
Neurons;
Apoptosis
- From:
Chinese Journal of Neurology
2010;43(12):878-882
- CountryChina
- Language:Chinese
-
Abstract:
Objective The effects of nemo-like kinase(NLK)in inflammation of central nervous system were explored. Methods An animal model with central nervous system inflammation disease induced by intracerebroventricular infusion of lipopolysaccharide was constructed. A model of neuronal apoptosis induced by glutamate in PC12 cells was constructed. A pcdna 3.1-NLK over-expression plasmid and a pSilencer 4. 1-CMV-NLK small interfering plasmid were also constructed. The expression and location of NLK were detected using western blot analysis, double immunofluorescent staining, and cell counting kit-8 assay. Results The protein level of NLK was reduced after induction of inflammation in the brain(t =2. 718-3. 106, all P ＜0. 01), and NLK was only expressed in both cortical and hippocampal neurons. At the cellular level, NLK expression was gradually reduced along with neuronal apoptosis induced by glutamate in PC12(t =4. 032, P ＜0. 01). Over-expression of NLK would reduce the apoptosis of neurons induced by glutamate(t =3. 930, P ＜ 0. 01). Conversely, interfering the expression of NLK would enhance neuronal apoptosis(t = 2. 845, P ＜ 0. 01). Conclusion NLK can protect neurons by inhibiting apoptosis in the process of central nervous system inflammation.
