The effect of Gαi2 on neuronal apoptosis in cerebral ischemia-reperfusion injury model of rats

Abstract

Objective To discuss the levels of inhibitory protein Gαi2 （Gcxi2） in hippocampus of brain and the effects of Gαi2 on neuronal intracellular Ca^2＋ level in cerebral ischemia reperfusion injury model of rats. Methods Ninety SD rats were randomly （ random number） assigned to sham group （ n = 30 ）, ischemic - reperfusion （IR） group （ n = 30）, Pertussis toxin （PT） group （ n = 30）. The blood flow of right common carotid artery of rat was blocked for 90 mix to make ischemia reperfusion model. The levels of Gαi2 in hippocampus was assayed by immunohistochemistry and Western blotting after ischemia reperfu - sion for 6, 12, 24 h in each group. The average fluorescence values of intracellular Ca^2＋ levels in hippocampus of rats in three groups were detected by using Flow CytoMeter （FCM）. Neuronal cell apoptosis was measured by TUNEL. Results After restoration of middle cerebral artery blood flow for different lengths of time, the levels of hippocampus God2 and Ca2 ＋ levels in IR group were significantly higher than those in Sham group （P 〈0. 01 ）. The hippocampus Ca^2＋ levels in PT group were higher than those in IR group （P 〈0. 01 ） . The apoptotic rates of neurons in PT group were lower than those in IR group （P 〈 0. 05 ）. Conclusions The level of Gαi2 in cerebral ischemia reperfusion injury model was increased. Gαi2 might reduce the calcium ion concentration of neurons after cerebral ischemia and reduce the neuronal cell apoptosis in this model. Gαi2 might play a role in protecting neuron from cerebral ischemia reperfusion Key words: Gαi2; Cerebral isehemia reperfusion injury; Hippocampus; Pertussis toxin; Apoptosis ; Neuron ; Ca^2＋ ; Death