Study on the neuroprotective role and its mechanism of p-nerve growth factor in rats with focal cerebral ischemia
10.3760/cma.j.issn.0254-9026.2009.01.022
- VernacularTitle:β-神经生长因子在脑缺血神经保护中作用机制的研究
- Author:
Leisi BIAN
;
Zhenguo LIU
;
Wenan WANG
- Publication Type:Journal Article
- Keywords:
Cerebral lschemia;
Tropomyosin;
Receptor protein-tyrosine kinases;
Protein kinases;
Nerve growth factor
- From:
Chinese Journal of Geriatrics
2009;28(1):74-77
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the dynamic changes of Trk(tropomyosin receptor kinase) and Akt(protein kinase B), and to explore the neuroprotective role and its mechanism of β-NGF (β-nerve growth factor) after focal cerebral ischemia. Methods A focal cerebral ischemia rat model was made and β-NGF was injected intra abdominally. The phosphorylation of Trk and Akt were tested by immunocytochemistry and Western blot assay. Results Trk receptor was increased obviously in the penumbra area after 8 h of infarction. The level of phosphorylated Trk(p-Trk) was increased after 2 h of infarction, while the level of phosphorylated Akt(p-Akt) had a decrease and then recovered gradually. The level of p Akt in cerebral ischemia group was decreased by 76.5% compared with that in control group after 8 h of infarction(P<0. 01). After the injection of β-NGF, the level of p-Trk was increased by 74.4% after 12 h of infarction(P<0.01), while the level of p-Akt was recovered significantly after 8 h of infarction, and had no statistical difference compared with the control group after 24 h of infarction (P>0.05). Conclusions Ischemia induces the activation and increased expression of Trk receptor, andβ-NGF may play a protective role in cerebral ischemia by increasing the phosphorylation of Trk and regulating the phosphorylation of Akt.
