摘要
目的:探讨3-硝基丙酸(3-NPA)预处理对海马脑片缺氧损伤的保护作用及线粒体内膜ATP敏感性钾(Mi-toK_(ATP))通道在预处理脑保护机制中的作用。方法:采用Nissl染色和透射电镜观察缺氧后大鼠海马CA_1区神经元密度、锥体细胞和亚细胞结构在预处理前后的变化,以及MitoK_(ATP)拮抗剂5-羟基癸酸盐(5-HD)孵育海马脑片对预处理效果的影响。结果:3-NPA组大鼠缺氧后海马CA_1区神经元密度(86.69±4.87)高于对照组(53.85±3.13,P<0.05),锥体细胞超微结构受损程度较对照组明显减轻。预处理大鼠海马脑片经100μmol/L 5-HD孵育后CA_1区神经元密度(57.31±7.89)较未孵育脑片降低(P<0.05),超微结构受损加重。结论:3-NPA预处理可提高海马脑片缺氧耐受能力,这种保护作用可能与MitoK_(ATP)通道开放有关。
Objective: To investigate the protective effect of 3-nitropropionic acid (3-NPA) and its relationship with the mitochondrial ATP-sensitive potassium (MitoKATP) channels. Mesthod: HE staining and the observing of the ultra-microscopic structure of the region CA1 was made after 15min hupoxia and 2h posthypoxic recovery in hippocampal slices of SD rats, which were pretreated in vivo with a single intraperitoneal injection of 3-NPA(20mg/kg). HE staining and the observing of the ultramicroscopic structure of the region CA1 were also made after perfusion with 5-hydroxyde-canoate, the mitochondrial KATP channel blocker. Results: 3-NPA caused an increase of the density of neurons of region CA1 from 53. 85±3. 13 in the control to 86. 69±4. 87 in the 3-NPA pretreated hippocampal slices and the decrease of the harm of the ultramicroscopic structure of region CA1. The protective effect of 3-NPA was blocked by 5-HD as shown by a decrease of the density of neurons of CA1 region to 57. 31±7. 89 and an increase of the harm of the ultramicroscopic structure of region CA1 5-HD had no proi schemic effect in control animals. Conclusions: 3-NPA induces anti-ischemic effect viaopening of mitochondrial KATP channels.
出处
《脑与神经疾病杂志》
2003年第4期193-197,共5页
Journal of Brain and Nervous Diseases
基金
国家教委回国人员启动基金(2001-345)
