Signal transducer and activator of transcription-3 activation after focal cerebral ischemia and reperfusion in rats
10.3760/cma.j.issn.1671-8925.2009.06.004
- VernacularTitle:大鼠局灶性脑缺血再灌注区域STAT3激活的实验研究
- Author:
Wen-Juan WU
1
;
Kai XU
;
Yu-Tao RONG
;
Hong MA
Author Information
1. 江苏省无锡市第二人民医院
- Keywords:
Cerebral ischemia and reperfusion;
STAT3
- From:
Chinese Journal of Neuromedicine
2009;8(6):556-559
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the activation of signal transducer and activator of transcription-3 (STAT3) in rats following focal cerebral ischemia/repeffusion (IR) and explore the correlation between STAT3 activation and the cerebral infract volume. Methods Ninety-nine SD rats were randomized into sham-operated group (n=9) and two IR groups with right middle cerebral artery occlusion with thread for 2 h (n=45) and 6 h (n=45) followed by reperfusion. At different time points after the end of the ischemia, the rats were sacrificed to obtain the brain tissue for triphenyltetrazolium chloride (TTC) staining to determine the infract volume. Immunohistochemistry and Western blot were used to detect the expressions of STAT3 and phosphorylated STAT3 (P-STAT3) in the brain tissue, and their correlations to the infarct volume were analyzed. Results Cerebral ischemia induced obvious infraction in the right hemisphere of the rats, where TTC staining was absent. Ischemia for 6 h resulted in more extensive areas without TTC staining than ischemia for 2 h (P<0.05). Reperfusion for 24 h after a 2-hour ischemia was associated with obviously reduced area free of TTC staining (P<0.05), whereas reperfusion for 24 h following a 6-hour ischemia only caused mild reduction of the TTC staining-free area. Immunohistochemistry of the brain tissue demonstrated the presence of STAT3 protein expression in the cytoplasm and P-STAT3 in the cell nuclei. IR was found to cause changes in the expression of P-STAT3 but not STAT3 protein, and the expression of P-STAT3 increased with the reperfusion time, reaching the peak level at 24 h of reperfusion. The activation level of STAT3 protein was inversely correlated to the dimension of the TTC staining-free area in the brain. Conclusion STAT3 is expressed in the cytoplasm and P-STAT3 in the cell nucleus of the brain tissue. Without causing obvious changes in STAT3 expression level, cerebral ischemia and reperfusion increases the phosphorylation level of STAT3 in inverse correlation to the size of the infarct area.
