| ObjectiveIncreasing evidence has shown that brain injury can develop as a result of cerebral ischemia - reperfusion due to stroke and other cardiovascular diseases. However, the mechanism on cerebral injury is not understood. The aim of this study is to investigate the protective effects and mechanisms of taurine on cerebral injury induced by brain ischemia/reperfusion in rats. It can provide a theories basis for its clinical application on cerebral viscular diseases.MethodsA middle cerebral artery occlusion model was establishe in Wistar rats and they were divided into three groups: sham group, ischemia - reperfusion group and ischemia - reperfusion with taurine treatment group. After ischemia 1hour and reperfusion 24hours in each model, the change in cerebral infarct volume, water content, pathologic alteration in brain tissues and the expression of Cyto-chrome c,Bcl -2 and Bax were determined.ResultsThe cerebral infarct volume percentage was 0, (13.32 ±3.18)%, (9. 21±2.24)% in the groups 1 ~3 respectively and it was reduced by 30. 83% in taurine treatment group compared with pure I/R group ( P <0. 05 ) . The brain water content was( 79.28 0.66 ) % , ( 82.46 0.94 ) % , ( 80.73 1.40 ) % in the three groups with a notable decrease in taurine treatment group ( P < 0. 05 ) . And likely, the ischemic neuronal damage was relieved and the expression of Cytochrome c and Bax protein were down regulated with taurine treatment ( P < 0. 05 ) . But the expression of Bel -2 was up regulated with taurine treatment ( P<0.05 ).ConclusionsTausine has a neuroprotective effect on reperfusion injury after focal cerebral ischemia in rats. Taurine markedly decreased the infarct size and ameliorated neurologic deficits score of rats subjected to MCAO. This effect is related to the inhibition of release of Cytochrome c , activated of Bax and the induced over-expression of Bel -2 . and the alleviation of neuronal damage. The participation of mitochondria in the mechanism of cell death may be that, the Bel - 2 family proteins could regulate the mitochondrial permeability transition, and/or the release of apoptogenic proteins , such as cytochrome c, to the cytoplasm where it activates caspase - 3, which has been reported to trigger apoptosis. |
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