Role of telomerase reverse transcriptase in focal cerebral ischemia reperfusion injury of rats with pre-stimulation of cerebellar fastigial nucleus
10.3760/cma.j.issn.1671-8925.2012.05.004
- VernacularTitle:端粒酶逆转录酶在预电刺激小脑顶核后大鼠局灶性脑缺血再灌注损伤中的作用
- Author:
Zhao-Xia ZHANG
1
;
Jing-Li LIU
;
Lei ZHANC
;
Yi YANG
;
Xiao-Ling WANG
;
Fei ZHU
;
Fang XIAO
Author Information
1. 广西医科大学第一附属医院
- Keywords:
Cerebral ischemia;
Telomerase reverse transcriptase;
Bax protein;
Electrical stimulation;
Fastigia nucleus;
Cell apoptosis
- From:
Chinese Journal of Neuromedicine
2012;11(5):448-453
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the effect of electrical pre-stimulation of cerebellar fastigial nucleus (FN) on protein expression of telomerase reverse transcriptase (TERT) in rats with focal cerebral ischemia and reperfusion and its mechanism of mitochondrial protection. Methods Adult male Wistar rats (n=150) were randomly divided into a vehicle group (2-hcerebral ischemia,followed by 24,48 and 72 h of reperfusion) and a FN stimulation group (electrical stimulation of the FN for 1-h daily before 2-h cerebral ischemia,followed by 24,48 and 72 h of reperfusion).TTC staining was employed to measure ischemic lesion volumes.Western blotting was used to observe TERT and Bax protein expressions.The apoptotic cells were detected by TUNEL assay. Transmission electron microscopy was employed to detect the changes of mitochondrial ultrastructure. Results The size of the cerebral infarct in the vehicle group was significantly larger than that in the FN stimulation group at all reperfusion time points (P＜0.05).The relative value of TERT protein expression in the FN stimulation group (0.87±0.51,0.91 ±0.40 and 0.80±0.24) was also obviously higher than that in the vehicle group (0.73±0.37,0.80±0.51 and 0.64±0.33) at all reperfusion time points (P＜0.05); however, a significantly reduced number of TUNEL-positive cells in the FN stimulation group (53.60±5.18,64.00±2.37 and 49.83±4.26) was noted as compared with that in the vehicle group (63.57±3.74,75.40±5.55 and 60.00±2.37) at all reperfusion time points (P＜0.05).No significant difference on Bax protein expression was noted between the vehicle group and FN stimulation group (P＞0.05).The degree ofmitochondrial damage in the FN stimulation group (1.50±0.41,1.75±0.52 and 1.33±0.52) was also significantly lower than that in the vehicle group (2.50±0.63,3.08±0.58 and 2.33±0.41) at all reperfusion time points (P＜0.05). Conclusion TERT protein expression is significantly increased following FN stimulation, which can reduce ischcmic neuronal apoptosis by protecting the mitochondrial dysfunction.
