The Role Of Tert In Rat Focal Cerebral Ischemia/Reperfusion Injury With PRE-Stimulation Of Cerebellal Fastigial Nucleus

Objective:To study the effect of cerebellar fastigial nucleus electrical stimulation on telomerase reverse transcriptase expression location and its possible mechanism of mitochondrial protection in rats with focal cerebral ischemia and reperfusion.Methods:Adult male Wistar rats (n=120) were randomly divided into two groups:a modeling group (2-hour cerebral ischemia, followed by24,48and72hours of reperfusion) and a FN-stimulating group (electrical stimulation of the FN for1-hour one day before2-hour cerebral ischemia, followed by24,48and72hours of reperfusion). Use the TTC staining to measure ischemic lesion volumes. The apoptotic cells were detected by TUNEL. Exert Western blot and immuno-electron microscopy method to observe TERT、Bax protein expression and location. Use transmission electron microscopy to detect the changes in mitochondrial ultra structure.Results:The size of the cerebral infarct was significantly greater in the modeling group than in the FN-stimulating group (P<0.05) at all reperfusion time points. Compared with the modeling group (63.57±3.74,75.40±5.55,60.00±2.37) the FN-stimulating group (53.6±5.18,64±2.37,49.83±4.26) had a significantly reduced number of TUNEL-positive cells (P<0.05). TERT protein relative expression in the FN-stimulating group (0.871±0.505,0.908±0.396,0.798±0.238) was also higher than the modeling group (0.727±0.366,0.796±0.510,0.642±0.325)(P<0.05), but in the FN-stimulating group most TERT located at the cytoplasm outside the mitochondrial(P<0.05. There was no significant difference between the modeling group and FN-stimulating group in Bax protein relative expression, but Bax location had changed:in the modeling group most Bax located at the mitochondrial; in the FN-stimulating group most Bax located at the cytoplasm outside the mitochondrial (P<0.05). The level of mitochondrial damage in the FN-stimulating group (1.50±0.41.1.75±0.52,1.33±0.52) was also significantly lower than the modeling group (2.50±0.63,3.08±0.58,2.33±0.41)(P<0.05).Conclusions:The results show that TERT protein expression was significantly increased following FN stimulation, the increased TERT protein can protect mitochondrial dysfunction-. reduce ischemic neuronal apoptosis maybe by change its location.