2007•Zhongguo yaolixue tongbaoRequires access
Effects of activating gamma-hydroxybutyric acid receptor on neuronal apoptosis following focal cerebral ischemia-reperfusion injury in rats
Dai Ti-jun
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Abstract
Aim To study the effect of gamma-hydroxybutyric acid receptor(GHBR ) on neuronal apoptosis suffering from focal cerebral ischemia-reperfusion injury in rats. Methods The male Sprague-Dawley rats weighing 240～280 g were randomly divided into seven groups: sham operation group(sham), ischemia-reperfusion group(Isc/R) ,NCS-356 160、320、640 μg·kg-1 group(N1、N2、N3),NCS-382 640+NCS-356 640 μg·kg-1 group(NCS-382+N3),and nimodipine 600 μg·kg-1 group(Nim).The middle cerebral artery occlusion(MCAO) model invented by Zea Longa with modifications was adopted. The experiment was divided into two parts after ischemia reperfusion for 24h:In the first part,we measured the cerebral expression of Bax, Bcl-2, Caspase-3 by immuneohistochemical method. In the second part,we measured neuronal apoptotic rate by flow cytometry in the ischemic cortex region. Results The expression rate of Bcl-2 and Bcl-2/Bax ratio of N1,N2,N3 and Nim groups were all higher than that of Isc/R group(P0.01);The expression rate of Bax, Caspase-3 and neuronal apoptotic rate in N2,N3,Nim groups were lower than that of Isc/R group(P0.05,P0.01). The expression rate of Bcl-2 positive neurons and Bcl-2/Bax ratio of NCS-382+N3 group were lower than that of N3(P0.05), whereas the expression rate of Bax, Caspase-3 and neuronal apoptotic rate were higher than that of N3(P0.05,P0.01). Conclusions The expression rate of Bcl-2 and Bcl-2/Bax ratio increased and the expression rate of Bax, Caspase-3 and neuronal apoptotic rate of ischemia neurons decreased after GHBR was activated by NCS-356, which could inhibit cell apoptosis following focal cerebral ischemia reperfusion injury in rats.