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纸质出版:2010
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范沁林,焦岩,刘国军,周振华,张波,陈林,甘立霞,陈康宁.大鼠全脑缺血再灌注后HAX-1蛋白与皮质神经元凋亡的关系[J].陆军军医大学学报(原第三军医大学学报),2010,32(06):584-587.
Fan Qinlin,Jiao Yan,Liu Guojun,Zhou Zhenhua,Zhang Bo,Chen Lin,Gan Lixia,Chen Kangning.Relationship between HAX-1 expression and neuron apoptosis after cerebral ischemia reperfusion injury in rats[J].J Amry Med Univ (J Third Mil Med Univ),2010,32(06):584-587.
范沁林,焦岩,刘国军,周振华,张波,陈林,甘立霞,陈康宁.大鼠全脑缺血再灌注后HAX-1蛋白与皮质神经元凋亡的关系[J].陆军军医大学学报(原第三军医大学学报),2010,32(06):584-587. DOI:
Fan Qinlin,Jiao Yan,Liu Guojun,Zhou Zhenhua,Zhang Bo,Chen Lin,Gan Lixia,Chen Kangning.Relationship between HAX-1 expression and neuron apoptosis after cerebral ischemia reperfusion injury in rats[J].J Amry Med Univ (J Third Mil Med Univ),2010,32(06):584-587. DOI:
目的 探讨大鼠全脑缺血再灌注后皮质组织中HAX-1蛋白(HS1-associated protein X-1
HAX-1) 与皮质神经元凋亡的关系。 方法 建立大鼠四血管法全脑缺血模型,将实验动物分为5组(n=5):正常组,缺血6、24、48、72 h组。采用HE染色,观察大鼠皮层组织病理变化;采用免疫组化、TUNEL法检测大鼠全脑缺血再灌注后HAX1蛋白的表达以及皮质神经元凋亡蛋白Caspase3的表达情况。 结果 HAX1蛋白在缺血后6 h表达最高(37.60±3.45),24、48、72 h降低[分别为(11.40±1.14)、(10.40±1.52)、(9.80±1.30)],且低于正常水平(P0.01);Caspase-3蛋白随着缺血时间的延长逐渐增高[6、24、48、72 h分别为(72.80±5.49)、(106.20±6.91)、(129.00±19.74)、(166.20±15.32)](P0.01),并伴随神经元凋亡的数目逐渐增加[(92.00±9.06)、(133.80±10.64)、(157.00±10.83)、(187.80±14.96)]。 结论 全脑缺血再灌注后皮质神经元中HAX-1蛋白在短期缺血中表达升高,可能参与神经元的抗凋亡,随着缺血时间延长,其表达水平降低,与神经元的凋亡增强相关。
Objective To investigate the relationship between HS1-associated protein X-1 (HAX-1) expression and neuron apoptosis in rats after global cerebral ischemia reperfusion injury. Methods Rats were subjected to global cerebral ischemia reperfusion injury through fourvessel occlusion
and then the experimental rats were divided into 5 groups
normal group (NC)
6
24
48 and 72 h post injury groups (n=5 for each group). Immunohistochemistry and TUNEL were used to detect HAX-1 expression and activated Caspase-3
and cell apoptosis in cortex of rats. Results The expression level of HAX1 in ischemic cortex was peaked at 6 h (37.60±3.45)
then decreased at 24
48 and 72 h (11.40±1.14
10.40±1.52
and 9.80±1.30 respectively)
to an extend lower than the normal level (P0.01). The expression of Caspase-3 in ischemic cortex was up-regulated after global cerebral ischemia reperfusion injury in rats with the prolongation of injury time (72.80±5.49
106.20±6.91
129.00±19.74
and 166.20±15.32 respectively for 6
24
48 and 72 h post injury). The number of apoptotic cells was increased obviously with the elapse of time (92.00±9.06
133.80±10.64
157.00±10.83
and 187.80±14.96 respectively for 6
24
48 and 72 h post injury
P0.01). Conclusion The expression of HAX-1 reachs a peak in a short time after global ischemia reperfusion injury
suggesting it may be involved in the anti-apoptosis of neuron apoptosis. With the elapse of injury time
its expression is decreased and associated with the increase of apoptotic cells.
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