摘要
目的研究厚朴酚(Magnolol,Mag)预处理对视网膜缺血再灌注损伤后神经元凋亡和bcl-2、caspase-3蛋白表达的影响,并探讨其对视网膜缺血保护的可能机制。方法用升高眼压的方法制作兔视网膜缺血模型,将新西兰大白兔随机分为正常组、生理盐水组及Mag组。缺血前24 h,对照组耳缘静脉注射生理盐水,Mag组注射厚朴酚100 mg/kg。观察缺血再灌注后不同时间段对照组及Mag组视网膜组织学变化,TUNEL检测及bcl-2、caspase-3蛋白的表达。结果视网膜缺血再灌注各时间段,HE染色Mag组大鼠视网膜内层厚度均较对照组厚,且内核层细胞数较多(P<0.01);TUNEL法检测正常组无凋亡细胞,缺血再灌注24 h凋亡达高峰,Mag组内核层的凋亡细胞比对照组少(P<0.01);Mag组和对照组在缺血再灌注12 h均检测到bcl-2、caspase-3蛋白表达,Mag组较生理盐水组少(P<0.01)。结论Mag预处理可以促进视网膜缺血再灌注后细胞的存留,减少细胞凋亡,bcl-2、caspase-3蛋白表达的调节可能参与这种保护机制。
Objective observe the effect of magnolol（Mag） pretreatment on bcl- 2 and caspase -3 expression after retinal ischemia and explore the neuro- protection mechanism of Mag. Methods The New Zealand rabbit model of experimental retinal ischemia was made by increasing the intraocular pressure. The rabbits were divided into normal group, saline group and Mag group randomly. Mag at 100 mg/kg or normal saline control was administered 24 hours before retinal ischemia. The histological changes,TUNEL detection and the expression of bcl-2 and caspase -3 protein in retina at different time - points after reperfusion were observed. Results The thickness of the inner retina and the INL cell number of Mag group were bigger than those of the saline group after HE staining during all the post - reperfusion stages（P 〈0.01 ） ;There were less apoptosis cells（P 〈0. 01 ）in Mag group than those in ischemia group at 24 hours after reperfusion ; The expression of bcl-2 and caspase -3 protein at 12 h after reperfusion between Mag group and control group was significantly different （P 〈 0.01 ） . Conclusion Magnolol pretreatment can promote neuronal viability, inhibit the apoptosis of neurons after retinal ischemia, and the down -regulating of bcl- 2 and caspase -3 expression might contribute to the protective mechanism.
出处
《湖北民族学院学报（医学版）》
2007年第1期14-17,20,共5页
Journal of Hubei Minzu University(Medical Edition)
基金
重庆市卫生局中医药科研项目基金(2005B71)
