经颈内动脉注射pLXSN-bcl-2对脑局灶性缺血再灌注大鼠脑组织的影响

目的:研究经颈内动脉注射pLXSN-bcl-2对大鼠脑缺血再灌注损伤后的影响。方法:51只健康成年Wistar大鼠随机分对照组、空质粒组、bcl-2组,每组分缺血再灌注9,24h两小组。采用线栓法制作大脑中动脉梗死模型,2h后实现再灌注。3h后经颈内动脉注射质粒pLXSN,pLXSN-bcl-2。检测缺血再灌注24h后大鼠脑梗死体积,及各组大鼠脑内bcl-2、caspase-3的表达情况和神经细胞凋亡情况。结果:bcl-2组缺血再灌注24h的脑梗死体积最小;bcl-2组在缺血再灌注9,24h后bcl-2阳性表达明显升高;缺血再灌注24h caspase-3蛋白表达及凋亡细胞数明显降低,缺血再灌注9h后与其他组之间无差异。结论:脑缺血再灌注3h后经颈内动脉注射pLXSN-bcl-2可以增加bcl-2在脑内的表达,并在缺血再灌注24h后通过抑制caspase-3的表达,抑制神经细胞凋亡,减少脑梗死体积。而在缺血再灌注9h尚未表现出明显的神经保护作用。

Effect of pLXSN-bcl-2 injected into internal carotid artery on brain tissue of rats after focal cerebral ischemia-reperfusion

Objective:To study the effect of pLXSN-bcl-2 injected into carotid artery on brain tissue of rats after focal cerebral ischemia-reperfusion.Methods:Fifty-one healthy adult Wistar rats were randomly and equally divided into control group,plasmid control group,and bcl-2 group,and in each group the rats were subdivided into 9-hour and 24-hour ischemia-reperfusion subgroups(n=6 and n=11,respectively).The left middle cerebral artery was occluded for 2 hours,and pLXSN or pLXSN-bcl-2 was injected into internal carotid artery 3 hours later.The cerebral infarct volume 24 hours after ischemia-reperfusion,the expressions of bcl-2 and caspase-3,and the apoptosis of neural cells were determined.Results:In bcl-2 group,the cerebral infarct volume 24 hours after ischemia-reperfusion significantly decreased,and the expression of bcl-2 significantly increased 9 and 24 hours after ischemia-reperfusion.No significant difference in the expression of caspase-3 and the apoptosis of neural cells was found between 3 groups 9 hours after ischemia-reperfusion,but the expression of caspase-3 and the apoptosis of neural cells in bcl-2 group significantly decreased 24 hours after ischemia-reperfusion.Conclusion:Injection of pLXSN-bcl-2 into internal carotid artery 3 hours after ischemia-reperfusion may reduce cerebral infarct volume by inhibiting the expression of caspase-3 and the apoptosis of neural cells 24 hours after ischemia-reperfusion,but no such effect exists 9 hours after ischemia-reperfusion.