摘要
目的观察脑缺血再灌注损伤后过氧化物酶体增殖物激活受体γ(PPARγ)表达对神经元凋亡的影响。方法日本大耳白兔72只,参照Pulsinelli四动脉阻断法建立兔全脑缺血90min/再灌注6h,1d,3d,7d,14d和28d的动物模型。TUNEL法染色观察脑皮质、海马和纹状体区神经元凋亡,免疫组织化学法检测PPARγ阳性神经元在各区的表达。结果脑缺血90min再灌注6h,1d,3d,7d,14d皮质、海马和纹状体区凋亡神经元明显增加(t皮质=3.86,P<0.01;t海马=4.96,P<0.01;t纹状体=2.91,P<0.05)。脑缺血再灌注6h,1d,3d,7d,14d,28d,PPARγ阳性神经元在各区明显增加(t皮质=7.98,P<0.01;t海马=7.65,P<0.01;t纹状体=6.98,P<0.01),其中再灌注6h,7d,14d,28d阳性神经元呈高值表达。结论脑缺血再灌注损伤后PPARγ表达能有效抑制神经元凋亡。
Objective To study the influence of peroxisome proliferator-activated receptor gamma （PPARγ） expression on neural apoptosis after cerebral ischemia reperfusion injury. Methods Total of 72 oryctolagus cuniculus were established models of global cerebral ischemia reperfusion injury of rabbits according to Pulsinelli＇s four arteries occlusion method. All animals were divided into six subgroups according to different reperfusion time point as 6 h, 1 d, 3 d, 7 d, 14 d and 28 d after 90 minutes ofischemia. The neural apoptosis in cortex, hippocampus and striatum were observed with TUNEL staining. The alterations of positive neuron of PPART in different area were detected with immunohistochemical method. Results The number of apoptotic neurons in cortex, hippocampus and striatum in the reperfusion 6 h, 1 d, 3 d, 7 d and 14 d subgroups increased more than those in the sham-operation group （tcontex = 3.86, P 〈0.01; thippocampus = 4.96, P 〈0.01; tstriatum= 2.91, P 〈0.05）. The positive neurons of PPART expressed in different area in reperfusion 6 h, 1 d, 3 d, 7 d, 14 d and 28 d subgroups increased obviously more than those in the sham-operation group （tcontex = 7.98, P 〈0.01; thippocampus = 7.65, P 〈0.01; tstristum = 6.98, P 〈0.01）. Conclusions PPARy expression can restrain the neuron apoptosis availably after ischemia/reperfusion injury in rabbits.
出处
《临床医学工程》
2012年第9期1472-1474,共3页
Clinical Medicine & Engineering
关键词
脑缺血
再灌注损伤
神经元
凋亡
PPARΓ
兔
Cerebral ischemia
Reperfusion injury
Neural apoptosis
PPARγ
Rabbits
