The Effects of 14-3-3 Phosphorylation Induced by JNK on Ischemic Brain Injury in Rats
10.3969/j.issn.0253-9896.2014.07.008
- VernacularTitle:JNK磷酸化14-3-3在大鼠缺血性脑损伤中的作用
- Author:
Xiaotian WANG
;
Xiaomei LIU
;
Renxian TANG
;
Hongjuan YOU
;
Xiaocui LI
;
Suping QIN
;
Yuanjian SONG
- Publication Type:Journal Article
- Keywords:
14-3-3 proteins;
JNK mitogen-activated protein kinases;
bcl-2-associated X protein;
brain ischemia
- From:
Tianjin Medical Journal
2014;(7):654-656
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of 14-3-3 phosphorylation (p-14-3-3) induced by C-Jun N-termi-nal kinase (JNK) on ischemic brain injury in rats. Methods Twenty rats were divided into 4 groups:sham operation group, ischemia-reperfusion group, SP600125 group and solvent control group. The rat model of cerebral ischemia was established. The p-14-3-3, the binding of 14-3-3 and Bax and the protein expression of Bax in cytoplasm and mitochondria in hippo-campal CA1 region were detected by immunoprecipitation (IP) and immunoblotting 12-hour after ischemia-reperfusion in four groups. Results Compared with the sham operation group, protein expression levels of p-14-3-3 in cytoplasm and Bax in mitochondria were significantly increased, the binding of 14-3-3 and Bax was significantly decreased in ischemia-re-perfusion group, solvent control group and SP600125 group. The protein expressions of p-14-3-3 and Bax were significantly lower in SP600125 group than those of ischemia-reperfusion group and solvent control group. The binding of 14-3-3 and Bax was significantly higher in SP600125 group than that of ischemia-reperfusion group and solvent control group (P <0.05). Conclusion 14-3-3 phosphorylation induced by JNK plays important effects on ischemic brain injury in rats.
