摘要
目的探讨Ⅱ相酶诱导剂CPDT(5,6-二氢环戊烯并1,2-二硫杂环戊烯-3-硫酮)对运动神经元的保护作用及机制。方法制作选择性运动神经元损伤的脊髓片培养模型。乳大鼠脊髓片分为正常对照组、模型组(100μmol/L苏-羟天冬氨酸;THA)和Ⅱ相酶诱导剂CPDT(5、15和30μmol/L)干预组。以神经元特异性抗体SM I-32组化染色,对脊髓腹角α运动神经元进行鉴定、计数,并测定不同时间点培养液中乳酸脱氢酶(LDH)及丙二醛(MDA)含量。结果THA使脊髓片腹角α运动神经元数目明显减少(P<0.01),培养液中LDH、MDA含量明显升高。与模型组相比,CPDT提前干预(15和30μmol/L)可使α运动神经元数目明显增多(P<0.05),突起也较为丰富,培养液中LDH、MDA含量明显下降(P<0.05)。结论Ⅱ相酶诱导剂CPDT可能通过抑制脂质过氧化物或清除自由基来保护脊髓选择性运动神经元不受损伤。
Objective To investigate the protection effect and mechanism of Phase Ⅱ enzyme inducer CPDT （5,6- dihydrocyclopenta [ C ]- 1,2-dithiole-3-thione） against threo-hydroxyaspartate-induced injury of motor neuron in the cultured spinal cord slices of rats. Methods Organotypic spinal cord slices of rat pup was divided into control group, model group（THA 100μmoL/L） and Phase Ⅱ enzyme inducer CPDT（5, 15, 30μmoL/L） treated groups. The morphology change of spinal cord slices was observed through inverted microscope. Ventral αmotor neurons＇ survivals were evaluated by immunohistochemical staining with monoclonal antibody SMI32, a nonphosphorylated neurof＇dament marker. Lactate dehydrogenase （LDH） and malonaldehyde （MDA） levels in culture medium were also measured. Results The slices of THA group showed that the number of Ventralαmotor neurons significantly decreased, but LDH enzyme activity and MDA level in culture medium increased. After CPDT（ 15, 30 μmoL/L） pretreatment, the spinal cord slices grew well and showed similar change with the slices of control group. The num-ber of α motor neurons significantly increased with intervention of CPDT as compared with model group. LDH and MDA level in culture medium decreased. Conclusion Phase Ⅱ enzyme inducer, CPDT may inhibit THA-induced motor neuron injury by inhibiting lipid superoxide and scavenging free radical.
出处
《基础医学与临床》
CSCD
北大核心
2007年第1期44-48,共5页
Basic and Clinical Medicine
基金
河北省自然科学基金(303487)
关键词
肌萎缩侧索硬化
Ⅱ相酶
运动神经元
器官型培养
模型
amyotrophic lateral sclerosis
Phase Ⅱ enzyme
motor neuron
organotypic culture
model
